Publication Spotlight

Celebrating the success of scientists citing Proteintech antibodies.

November feature papers
Unravelling an unsuspected role of a cellular protein in orchestrating viral RNA production

SND1 binds SARS-CoV-2 negative-sense RNA and promotes viral RNA synthesis through NSP9

Schmidt et al., Cell

Products cited: SND1 Mouse MonoAb, SND1 Rabbit PolyAb, HA Tag Mouse MonoAb, V5-Trap® Magnetic Agarose.

Novel kinase regulates mitochondrial gene expression

Regulators of mitonuclear balance link mitochondrial metabolism to mtDNA expression

Kramer et al., Nature Cell Biology

Products cited: TOMM40 Rabbit PolyAb, MRPS18B Rabbit PolyAb, MRPL12 Rabbit PolyAb, WBSCR16 Rabbit PolyAb, ATP6 Rabbit PolyAb, CYTB Rabbit PolyAb, CHCHD4 Rabbit PolyAb, TACO1/CCDC44 Rabbit PolyAb, TRUB2 Rabbit PolyAb.

TDP-43 pathologically spreads across neuro-glial connections connections in motor ccircuitry

TDP-43 differentially propagates to induce antero- and retrograde degeneration in the corticospinal circuits in mouse focal ALS models

Tsubogucji et al., Acta Neuropathology

Products cited: TDP-43 (C-terminal) Rabbit PolyAb

eNAMPT as a novel immunotherapeutic target for triple negative breast cancer

Extracellular nicotinamide phosphoribosyltransferase (eNAMPT) neutralization counteracts T cell immune evasion in breast cancer

Travelli et al., The Journal for Immunotherapy of Cancer

Products cited: PD-1 Mouse MonoAb, PD-L1 Mouse MonoAb

October feature papers
Novel pathway for m6A deposition on chromatin associated RNA with therapeutic implications for leukemia

RBFOX2 recognizes N6-methyladenosine to suppress transcription and block myeloid leukaemia differentiation

Dou et al., Nature Cell Biology

Products cited: FOX2/RBM9 Rabbit PolyAb, RBM15 Rabbit PolyAb

Unprecedented interplay between actin and mTORC1 signaling on the endolysosomal system

Codependencies of mTORC1 signaling and endolysosomal actin structures

Priya et al., Science Advances

Products cited: DYKDDDDK Fab-Trap™ Agarose, GFP-Trap® Agarose, Binding Control Agarose Beads

Unravelling the functions of PARP14

PARP14 is a PARP with both ADP-ribosyl transferase and hydrolase activities

Đukić et al., Science Advances

Products cited: DDX3 Mouse McAb, DDX6 Rabbit PolyAb, GFP-Trap® Magnetic Agarose

Ketone bodies are essential fuels for CD8+ T cells

Ketolysis drives CD8+ T cell effector function through effects on histone acetylation

Luda et al., Immunity

Products cited: BDH1 Rabbit PolyAb, OXCT1 Rabbit PolyAb

September feature papers
Proteomics breakthrough: A method for mapping endogenous protein trafficking

Dynamic mapping of proteome trafficking within and between living cells by TransitID

Wei et al., Cell

Products cited: CYTB Rabbit PolyAb, EIF2AK2 Rabbit PolyAb, MTCO2 Rabbit PolyAb, MTCO3 Rabbit PolyAb, ND1 Rabbit PolyAb, ND5 Rabbit PolyAb.

Early developmental DNA crosslink repair acts as a failsafe to prevent retrotransposition

Fanconi anemia DNA crosslink repair factors protect against LINE-1 retrotransposition during mouse development

Bona et al., Nature Structural & Molecular Biology

Products cited: DCLRE1B Rabbit PolyAb, XRCC2 Rabbit PolyAb, XRCC3 Rabbit PolyAb.

Stress granule component inhibits Tau aggregation

Increased G3BP2-Tau interaction in tauopathies is a natural defense against Tau aggregation

Wang et al., Neuron

Products cited: TDP-43 (human specific) Mouse McAb, TDP-43 Rabbit PolyAb, Lamin B1 Mouse McAb, HA-Tag Mouse McAb, GFP tag Mouse McAb.

TIGIT inhibitory mechanism on T cells revealed

TIGIT can inhibit T cell activation via ligation-induced nanoclusters, independent of CD226 co-stimulation

Worboys et al., Nature Communications

Products cited: ChromoTek GFP-Booster ATTO488, ChromoTek GFP-Booster Alexa Fluor® 488, ChromoTek GFP-Booster Alexa Fluor® 647.

August feature papers
PLSCR1 discovered as a potent anti-SARS-CoV-2 defence factor

PLSCR1 is a cell-autonomous defence factor against SARS-CoV-2 infection

Xu et al., Nature

Products cited: PLSCR1 Rabbit PolyAb, TMEM41B Rabbit PolyAb, IFITM3 Rabbit PolyAb, GAPDH Mouse McAb, GFP tag Mouse McAb, Halo Monoclonal antibody (28A8)

Circulating tumor cell dynamics predict response overall survival for breast cancer

Dynamic glycoprotein hyposialylation promotes chemotherapy evasion and metastatic seeding of quiescent circulating tumor cell clusters in breast cancer

Dashzeveg et al., Cancer Discovery

Products cited: ALCAM Rabbit PolyAb, PAI-1 Rabbit PolyAb

Novel small inhibitor discovered for key protein involved in mitochondrial dysfunction

Targeting an allosteric site in dynamin-related protein 1 to inhibit Fis1-mediated mitochondrial dysfunction

Rios et al., Nature Communications

Products cited: FIS1 Rabbit PolyAb, MFF Rabbit PolyAb, KLF5 Rabbit PolyAb

Albumosomes have mitochondrial protective functions in hepatocytes

Albumosomes formed by cytoplasmic pre-folding albumin maintain mitochondrial homeostasis and inhibit nonalcoholic fatty liver disease

Ma et al., Signal Transduction and Targeted Therapy

Products cited: ACSL1 Rabbit PolyAb, FH Rabbit PolyAb, NDUFV1 Rabbit PolyAb, UQCRC1 Rabbit PolyAb, ATP8 Rabbit PolyAb

July publication spotlight: Ubiquitin drives ER-phagy | Two collaborative Nature papers highlight important finding

Great things come from collaborative science!

ER-phagy is a vital process for cellular homeostasis. In a long-standing collaboration between two German research groups lead by Prof Đikić at Frankfurt University and Dr Hübner at Jena University previously shown that defects in ER-phagy receptors cause rare neurodegenerative diseases.

Now, these two groups have concurrently published two papers in Nature demonstrating that ubiquitination of ER-

shaping proteins is vital for the correct regulation of ER-phagy.


Ubiquitination regulates ER-phagy and remodelling of endoplasmic reticulum

Gonzalez et al. Nature. PMID: 37225996 – Open access.

Heteromeric clusters of ubiquitinated ER-shaping proteins drive ER-phagy

Foronda et al., Nature. PMID: 37225994 – Open access.

These two groups used a fantastic 13 Proteintech products in their research!

Product Name

Catalog No.

Product Name

Catalog No.

AMFR/GP78 Rabbit PolyAb


REEP2 Rabbit PolyAb


ATL2 Rabbit PolyAb


REEP5 Rabbit PolyAb


ATL3 Rabbit PolyAb


RTN2 Rabbit PolyAb


CKAP4 Rabbit PolyAb


RTN3 Rabbit PolyAb


FAM134B Rabbit PolyAb


GFP-Trap® Agarose


GFP Monoclonal antibody


Myc-Trap® Agarose


REEP1 Rabbit PolyAb




June publication spotlight: 200,000 citations special!

We are thrilled to have reached the 200,000 citation milestone for Proteintech Group products! Huge thank you to everyone who has purchased and published with us. We are so proud of the achievements of our customers and to honored play a part in contributing to scientific knowledge.

To celebrate, we have highlighted one landmark paper published by Dr. David Liu’s team from Harvard Medical School recently released in Science by Arbab et al., “Base editing rescue of spinal muscular atrophy in cells and in mice” (PMID 36996170). Below is a summary of their findings written by Amanda Balboa Ramilo, a Vascular Biology PhD researcher at Uppsala University in Sweden.

Spinal Muscular Atrophy (SMA), the leading genetic cause of infant mortality, is a condition caused by homozygous loss or mutation in the Survival Motor Neuron 1 (SMN1) gene that results in a deficiency of the Survival Motor Neuron (SMN) protein. Reduced levels of SMN in humans cause progressive loss of motor neurons, paralysis, and death. Pharmacological treatment is fundamental to increase the life span of patients with SMA but current approved therapies, although efficient, have several limitations. In this paper, Arbab and colleagues propose a new therapeutic modality that restores endogenous SMN gene and protein expression while preserving native SMN regulation through a one-time permanent treatment, addressing the limitations of the current treatment options.

In patients with SMA, the loss of SMN1 is compensated by the presence of one or more copies of SMN2. These two genes share 99.9% sequence identity, differing only in nucleotide position 6 of exon 7 (CG to TA substitution). This substitution results in the truncated protein SMNΔ7, which is rapidly degraded and does not restore SMN function. In this paper, the authors explore several approaches to editing SMN2 in order to produce the functional SMN protein. Several nuclease and base editing strategies were evaluated in vitro. The most efficient strategy identified was the base editing of SMN2 splicing regulatory elements, achieving 94 to 95.5% conversion of AT to GC in nucleotide 6 of exon 7. This resulted in a 38-fold increase of SMN compared to untreated controls, corresponding to a 95% recovery of native SMN protein levels. This strategy also showed high efficiency and on-target precision. The off-target change identified has no anticipated physiological significance.

To test the in vivo effects of this strategy, the Adeno-Associated Virus Serotype 9 was used for delivery of the base editor to Δ7SMN neonate mice by intracerebroventricular injection. There was an 87± 2.7% conversion of AT to GC in nucleotide 6 of exon 7 among transduced cells and high single nucleotide precision, with few undesirable by-products. To maximize the effectiveness of SMA treatment in improving motor function and increasing life expectancy, it must be administered before the onset of neuromuscular symptoms. Δ7SMN mice have an extremely short therapeutic window (treatment is necessary from postnatal day 4 to 6), which is incompatible with the time needed for the base editing strategy to have an effect (1 to 3 weeks). Despite this, in this case, base editing promoted the maintenance of neuron motor functional integrity and a moderate increase in life span (from 17 to 23 days). To extend the therapeutic window of the strategy proposed, the authors suggest the co-administration of nusinersen (an SMA-approved drug) along with the base editor. Combination treatment increased the life span of the mice from 17 to 111 days.

In conclusion, the authors present a new efficient base editing strategy that with just one administration can increase SMN protein levels, prevent neuron motor function loss, and increase life span in mice.

Proteintech products

Arbab et al. used SMN Human-Specific monoclonal antibody (Cat# 60154-1-Ig, clone# 2C6D9) and SMN-Exon7 monoclonal antibody (Cat# 60255-1-Ig, clone# 3A8G1) from Proteintech, and we are thrilled to have helped their research. 

May feature papers
Direct antibody labeling enables high-impact science

As scientists, we always remember that feeling of having our first paper published and seeing our name in print. At Proteintech, we have that same happy feeling as our collective efforts in developing the FlexAble antibody labeling kits have been rewarded with two publications by customers in high-impact journals!

BCAT2 is a potential target to treat bladder cancer in combination with immunotherapy

BCAT2 Shapes a Noninflamed Tumor Microenvironment and Induces Resistance to Anti‐PD‐1/PD‐L1 Immunotherapy by Negatively Regulating Proinflammatory Chemokines and Anticancer Immunity

Cai et al., 2023. Advanced Science

Products cited: FlexAble CoraLite®488 Antibody Labeling Kit for Rabbit IgG and CCL3, CCL4, CCL5, CXCL9, and CXCL10/IP10 Human ELISA kits.

How was FlexAble used?

Cai and colleagues used FlexAble to directly label their preferred BCAT2 antibody for flow cytometry analysis of murine tumors. FlexAble removed the need to use a secondary antibody in absence of a readily conjugated primary antibody.

Image right of flow data using FlexAble kit in Cai et al. publication (open source). 

New discoveries in osmoregulatory mechanisms in freshwater fish

Shih et al., 2023. International Journal of Molecular Sciences

Products cited: FlexAble CoraLite® Plus 647 Antibody Labeling Kit for Rabbit IgG and ATP6V1A Polyclonal antibody.

How was FlexAble used?

Shih and colleagues used FlexAble to directly label our Rabbit polyclonal to the VHa subunit Atp6v1a in fish gills. This enabled the team to also use their custome Ncc2 rabbit polyclonal in the same samples for multiplexing.

Image right of the immunofluorescent multiplex analysis of fish gills from Shih et al., (open source).

April feature papers
Autophagy in the liver is essential for benefits of exercise
Exercise-activated hepatic autophagy via the FN1-α5β1 integrin pathway drives metabolic benefits of exercise

Kuramoto et al. Cell Metabolism

Products cited: Human BCL2 Rabbit PolyAb

Novel epigenetic pathway for glucoeogenesis activation during fasting
Histone phosphorylation integrates the hepatic glucagon-PKA-CREB gluconeogenesis program in response to fasting

Meng et al. Molecular Cell

Products cited: PCK1 Rabbit PolyAb, G6PC Rabbit PolyAb, PPP2CA Rabbit PolyAb, DYKDDDDK tag Rabbit PolyAb, PKA C-alpha specific Rabbit PolyAb, YWHAZ Rabbit PolyAb, GFP tag Rabbit PolyAb

Intestine derived hormone promoted gluconeogenesis and ketogenesis during fasting
Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796

Long at al. Cell Research

Products cited: FURIN Rabbit PolyAb, Chromogranin B Rabbit PolyAb

Axonal guidance molecule Sema7a plays an inhibitory role in adipogenesis
Sema7a protects against high-fat diet-induced obesity and hepatic steatosis by regulating adipo/lipogenesis

Lu et al. Molecular Metabolism

Products cited: SEMA7A Rabbit PolyAb

March feature papers
Suppression of spliceosome-associated factors to treat a wide range of ALS forms
SYF2 suppression mitigates neurodegeneration in models of diverse forms of ALS 

Linares et al. Cell Stem Cell 

Products cited: CoraLite®594-conjugated Mu Crystallin Rabbit PolyAb, TDP-43 Rabbit PolyAb, Phospho-TDP43 (Ser409/410) Rabbit PolyAb, GR repeat Rabbit PolyAb, PR repeat Rabbit PolyAb 

Artificial light at night may lead to metabolic disorders
Light modulates glucose metabolism by a retina-hypothalamus-brown adipose tissue axis

Meng et al. Cell 

Products cited: BDNF Mouse MonoAB  

Chromatin modifier linked to developmental failures in neural crest cells and cartilage formation
The H2A.Z and NuRD associated protein HMG20A controls early head and heart developmental transcription programs 

Herchenröther at al. Nature Communications 

Products cited: HMG20A Rabbit PolyAb, HMG20B Rabbit PolyAb, KIAA0182 Rabbit PolyAb, BRD2 Rabbit PolyAb, GFP-Trap® Agarose. 

Novel complex regulates membrane lipid saturation through SREBP1-SCD1 pathway
The p97-UBXD8 complex regulates ER-Mitochondria contact sites by altering membrane lipid saturation and composition 

Ganji et al. Nature Communications 

Products cited: FAF2 Rabbit PolyAb, ACSL4/FACL4 Rabbit PolyAb, UBXD2 Rabbit PolyAb, HRD1/SYVN1 Rabbit PolyAb, SEC61B Rabbit PolyAb, Calnexin Rabbit PolyAb, UBXN1 Rabbit PolyAb, SREBF1 Rabbit PolyAb, SREBF2 Rabbit PolyAb, FADS1 Rabbit PolyAb, GFP tag Mouse McAb, AMFR/GP78 Rabbit PolyAb, GRP75 Rabbit PolyAb, VAPB Rabbit PolyAb, SCD Rabbit PolyAb, VCP Rabbit PolyAb 

February feature papers
Novel mechanism defining lipid utilization during thermogenesis
CLSTN3β enforces adipocyte multilocularity to facilitate lipid utilization

Qiang et al. Nature

Products cited: CLSTN3 Rabbit PolyAb, CIDEA Rabbit PolyAb, Tim23 Rabbit PolyAb, TOM20 Rabbit PolyAb, Ubiquitin Rabbit PolyAb.


Palmitoylation proteomics identifies role for ATP1 in T2 diabetes onset
Palmitoylation couples insulin hypersecretion with β cell failure in diabetes

Dong et al. Cell Metabolism

Products cited: CKAP4 Rabbit PolyAb, Myc-Trap® Magnetic Agarose, GFP-Trap® Magnetic Agarose.

MCC950, an NLRP3 inflammasome inhibitor, protects against podocyte damage in diabetic nephropathy
Inhibition of NLRP3 inflammasome ameliorates podocyte damage by suppressing lipid accumulation in diabetic nephropathy

Wu et al. Metabolism

Products cited: SOD1 Rabbit PolyAb, SOD2 Rabbit PolyAb, NOX4 Rabbit PolyAb, Beta Actin Mouse McAb.

Elucidation of surveillance pathway degrading eEF1A by two previously uncharacterised E3 ligases
An E3 ligase network engages GCN1 to promote the degradation of translation factors on stalled ribosomes

Oltion et al. Cell

Products cited: RPS13 Rabbit PolyAb, GFP-Trap® Magnetic Agarose.

January feature papers
Lipid phosphatase MTM1 reshapes the ER and increases mitochondrial networks
Read here (access required): Endosomal lipid signaling reshapes the endoplasmic reticulum to control mitochondrial function

Jang et al. Science

Products cited: RPL26 Rabbit PolyAb, RPL7 Rabbit PolyAb, KTN1 Rabbit PolyAb, RRBP1 Rabbit PolyAb, MFN1 Rabbit PolyAb, MFN2 Rabbit PolyAb, OPA1 Rabbit PolyAb, CHOP Rabbit PolyAb, ATG5 Rabbit PolyAb.


SYT3 is the previously unknown high-affinity Ca2+ sensor driving vesicle replenishment in neuronal synapses
Read here (access required): Fast resupply of synaptic vesicles requires synaptotagmin-3

Weingarten at al. Nature

Products cited: Synaptophysin Rabbit PolyAb, Syntaxin 1A / Syntaxin 1B Mouse McAb, HRP-Goat Anti-Rabbit IgG(H+L) SecondaryAB, HRP-Goat Anti-Mouse IgG(H+L) Secondary AB, HRP-Goat Anti-Guinea pig IgG(H+L) SecondaryAB.

Using genome wide knockout screens to in multiple cell lines to identify viral host regulators
Read here (access required): Bidirectional genome-wide CRISPR screens reveal host factors regulating SARS-CoV-2, MERS-CoV and seasonal HCoVs

Rebendenne et al. Nature Genetics

Products cited: ACE2 Rabbit PolyAb, AP1B1 Rabbit PolyAb.

Critical role for amino acid sensing pathways in colorectal cancer
Read here (access required): Dysregulated Amino Acid Sensing Drives Colorectal Cancer Growth and Metabolic Reprogramming Leading to Chemoresistance

Solanki et al. Gastroenterology

Products cited: Beta Actin Mouse McAb, Sestrin 2 Mouse McAb.


December Publication Spotlight, celebrating 170,000 product citations!
Special paper feature: Novel mechanism of acentrosomal spindle assembly in human oocytes

A recent publication in Science by Lei Wang’s group at Fudan University uncovered a unique mechanism for microtubule assembly and segregation in during human oocyte cell division. During mitosis, cells use the microtubule organizing centre (MTOC) to prepare for cell separation by the action of the centrosomes. This process is not well defined in meiosis (division of gametes) where there are no centrosomes and microtubule assembly differs between species. Using immunofluorescence and high-resolution imaging, Wang et al. identify a unique protein complex responsible for acentrosomal spindle assembly during meiosis in human oocytes. They have termed it the human oocyte microtubule organizing center (huoMTOC), it is formed of four key proteins CCP110, CKAP5, DISC1 and TACC3. The huoMTOC has clinical significance as this research also identifies mutations in TACC3 responsible for impaired oocyte maturation resulting in clinical infertility.

The authors cited 46 of our antibodies for immunofluorescence, breaking the record for the number of Proteintech product citations in a single publication. This takes Proteintech’s total product citations to over 170,000! We are honored for the team’s trust in our products and celebrate our customers’ research successes.

Table of cited antibodies in Wang et al. 2022




Aurora A







DCTN1/p150 glued






































November feature papers
C9orf72 and TBK1 mutations converge to induce to TDP-43 pathology in FTD-ALS
Two FTD-ALS genes converge on the endosomal pathway to induce TDP-43 pathology and degeneration

Shao et al., Science

Products cited:  TDP-43 (C-terminal) Rabbit PolyAb.

Novel mechanism detailing how C9orf72 mutation leads to neurodegeneration
C9orf72 functions in the nucleus to regulate DNA damage repair

He et al., Cell Death and Differentiation

Products cited: C9orf72 Rabbit PolyAb, KU70 Rabbit PolyAb, LIG4 Rabbit PolyAb.

Signaling pathway in reactive astrocytes following brain hemorrage leads to BBB breakdown
Astrocytic NDRG2-PPM1A interaction exacerbates blood-brain barrier disruption after subarachnoid hemorrhage

Feng at al., Science Advances

Products cited: Occludin Mouse McAb, ZO-1 Mouse McAb, MMP9 (N-terminal) Rabbit PolyAb, HA Tag Mouse McAb, DYKDDDDK tag Mouse McAb, HA tag Rabbit PolyAb, MPO Rabbit PolyAb, NDRG2 Mouse McAb.

Alternative mechanism on how progranulin deficiency leads to lysosomal dysfunction contributing to dementia
Deficiency of the frontotemporal dementia gene GRN results in gangliosidosis

Boland et al., Nature Communications

Products cited:  Galc Rabbit PolyAb, Alpha Galactosidase A Mouse McAb, GM2A Rabbit PolyAb, PSAP Rabbit PolyAb, Beta Galactosidase Rabbit PolyAb, HEXA Rabbit PolyAb, HSP90 Mouse McAb, TFE3 Rabbit PolyAb, P62,SQSTM1 Rabbit PolyAb, NDP52 Rabbit PolyAb, GABARAP Rabbit PolyAb, ASAH1 Rabbit PolyAb, HEXB Rabbit PolyAb.

October featured papers
Unbiased proteomic approach demonstrates novel protective mechanism in lysosomal dysfunction
A phosphoinositide signalling pathway mediates rapid lysosomal repair

Tan & Finkel, Nature

Products cited:  Galectin-3 Rabbit PolyAb, ATG2B Rabbit PolyAb, ATG2A Rabbit PolyAb, PI4K2A Rabbit PolyAb, OSBP Rabbit PolyAb, OSBPL9 Rabbit PolyAb, STAMBP Rabbit PolyAb, PI4KA Rabbit PolyAb, hIST1 Rabbit PolyAb, STAM Rabbit PolyAb.

Challenging dogma: discovery of membrane potential independent mechanisms of mitophagy
Protein import motor complex reacts to mitochondrial misfolding by reducing protein import and activating mitophagy

Micheaelis et al., Nature Communications

Products cited: Tim23 Rabbit PolyAb, PAM16 Rabbit PolyAb, GRPEL1 Rabbit PolyAb, LONP1 Rabbit PolyAb, TIMM44 Rabbit PolyAb.

Bringing the target up to PAR
Poly(ADP-ribose) promotes toxicity of C9ORF72 arginine-rich dipeptide repeat proteins

Gao et al., Science Translational Medicine

Products cited: TDP-43 (C-terminal) Rabbit PolyAb, PR Rabbit PolyAb, Glucocorticoid receptor Rabbit PolyAb, GFP-Trap® Agarose.

Expanding MINIFLUX to a three-colour channel with DNA labelling

Ostersehlt et al., Nature Methods

Products cited: Mitofilin Rabbit PolyAb

September featured papers
ASGR1 inhibition offers potential avenue for new cholesterol lowering therapies
Inhibition of ASGR1 decreases lipid levels by promoting cholesterol excretion

Wang et al., Nature

Cited products: ABCG5 Rabbit PolyAb, ACC1 Mouse McAb, ASGR1 Rabbit PolyAb,  AMPK Alpha 1 Rabbit PolyAb, AMPK Alpha 2 Rabbit PolyAb, CDC25C Rabbit PolyAb, FASN Rabbit PolyAb, GAPDH Rabbit PolyAb, PCNA Rabbit PolyAb, Raptor Rabbit PolyAb, ULK1 Rabbit PolyAb

Cytoplasmic METTL3 accumulation regulates translation initiation to drive gastric cancer progression
METTL3 preferentially enhances non-m6A translation of epigenetic factors and promotes tumourigenesis

Wei et al., Nature Cell Biology

Cited products: FBL Rabbit PolyAb, GAPDH Mouse McAb, HSP90 Rabbit PolyAb, Lamin B1 Mouse McAb, PCBP2 Rabbit PolyAb, RPL36 Rabbit PolyAb 

New population of autophagy-dysregulated astrocytes revealed in the aging mouse brain
A distinct astrocyte subtype in the aging mouse brain characterized by impaired protein homeostasis

Lee et al., Nature Aging

Cited products: GSTM1 Rabbit PolyAb, SCRG1 Rabbit PolyAb 

PCGF6 identified as a lineage switcher in human pluripotent stem cell differentiation
PCGF6 controls neuroectoderm specification of human pluripotent stem cells by activating SOX2 expression

Lan et al., Nature Communications

Cited products: Alpha Tubulin Rabbit PolyAb,  EHMT2 Mouse McAb, GAPDH Mouse McAb, MAX Rabbit PolyAb, PCGF6 Rabbit PolyAb, RYBP Rabbit PolyAb

August featured papers
Obesity is a driving force behind stress granule tumor dependence
Stress Granules determine the Development of Obesity-associated Pancreatic Cancer

Fonteneau et al., Cancer discovery

Products cited:  SRPK2 Rabbit PolyAb, KI67 Rabbit PolyAb

Discovery of the novel zygotene cilium in oocytes is a critical player in meiosis
Control of meiotic chromosomal bouquet and germ cell morphogenesis by the zygotene cilium

Mytlis et al., Science

Products cited: ARL13B Rabbit PolyAb

Using cryo-electron microscopy to determine the 3D structure of the human GATOR2 complex
Structure of the nutrient-sensing hub GATOR2

Valenstein et al., Science

Products cited: SEC13 Rabbit PolyAb, WDR24 Rabbit PolyAb, KPTN Rabbit PolyAb, NRF2, NFE2L2 Rabbit PolyAb

Novel mechanism in Huntington disease offers new therapeutic avenue
Mutant Huntington stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease

Eshraghi et al., Nature

Products cited: MGP Rabbit PolyAb, PPBP,NAP2 Rabbit PolyAb, Aggrecan Rabbit PolyAb, MFSD10 Rabbit PolyAb, TPPII Mouse McAb

July featured papers
Historical neurodegeneration finding – previously unsolved amyloid fibril is TMEM106B
Homotypic fibrillization of TMEM106B across diverse neurodegenerative diseases

Andrew Chang et al., Cell

Products cited:   TDP-43

Breakthrough in understanding the huge molecular diversity of astrocytes in response to different pathological conditions
Divergent transcriptional regulation of astrocyte reactivity across disorders.

Burda et al., Nature

Products cited: ATF2-Specific Rabbit PolyAbBCL3 Rabbit PolyAbCUX1 Rabbit PolyAbEBF1 Rabbit PolyAbELF1 Rabbit PolyAbESRRB Rabbit PolyAbFEV Rabbit PolyAbFUS/TLS Rabbit PolyAbGATA2 Rabbit PolyAbGATA4-Specific Rabbit PolyAbGFI1 Rabbit PolyAbHEXIM1 Rabbit PolyAbHOXC8 Rabbit PolyAbIRF9 Rabbit PolyAbKLF13 Rabbit PolyAbMYCN Rabbit PolyAbMYOD1 Rabbit PolyAbNFYA Rabbit PolyAbNOTCH1 Rabbit PolyAbB23/NPM1 Rabbit PolyAbNR2F1 Rabbit PolyAbPBX1 Rabbit PolyAbPITX1 Rabbit PolyAbRXRA Rabbit PolyAbSNAI1 Rabbit PolyAbSND1 Rabbit PolyAbSREBF1 Rabbit PolyAbSTAT3 Rabbit PolyAbSTAT4 Rabbit PolyAbTCF4 Rabbit PolyAbTGM1 Rabbit PolyAbp63 Rabbit PolyAbXRN2 Rabbit PolyAbYAP1 Rabbit PolyAb

Single cell analysis of human brain metastatic tumour cells reveals two functional archetypes
Cellular architecture of human brain metastases.

Gonzalez et al., Cell

Products cited: PEG10 Rabbit PolyAbS100A6 Rabbit PolyAb

Uncovering key mechanisms underlying DDX3X syndrome in intellectual disability
Pathogenic DDX3X Mutations Impair RNA Metabolism and Neurogenesis during Fetal Cortical Development.

Lennox et al., Neuron

Products cited: DDX3 Rabbit PolyAb

Phosphorylated TDP43 is found in ALS patients’ intramuscular nerve bundles
TDP-43 Accumulation Within Intramuscular Nerve Bundles of Patients With Amyotrophic Lateral Sclerosis.

Kurashige et al., JAMA Neurology

Products cited: Phospho-TDP43 (Ser409/410) Rabbit PolyAbTDP-43 (C-terminal) Rabbit PolyAb

June featured papers
Novel inhibitor effective in CCNE1-amplified cancer models
CCNE1 amplification is synthetic lethal with PKMYT1 kinase inhibition

Gallo et al., Nature

​Products cited: ChromoTek Cell Cycle Chromobody® plasmid (TagRFP)

SCREWs and NUTs regulate plant stoma opening
Phytocytokine signalling reopens stomata in plant immunity and water loss

Liu et al., Nature

Products cited: GFP-Trap® Agarose

Cross species network analysis of basement membrane proteins of human with animal models provides novel insights
A basement membrane discovery pipeline uncovers network complexity, regulators, and human disease associations (cover feature)

Jayadev et al., Science Advances

Products cited: Matrilin 2 Polyclonal antibody

Novel nanosystem for site-specific delivery of combined cancer immunotherapies
The programmed site-specific delivery of LY3200882 and PD-L1 siRNA boosts immunotherapy for triple-negative breast cancer by remodeling tumor microenvironment

Zhang et al., Biomaterials

Products cited: Mouse TGF-beta1 ELISA KitMouse CXCL9/MIG ELISA KitMouse TNF-alpha ELISA KitMouse IFN-gamma ELISA Kit

May featured papers
Clueless Mitochondria
Clueless/CLUH regulates mitochondrial fission by promoting recruitment of Drp1 to mitochondria. 

Yang et al. Nature Communications

Products cited: MFN2 Rabbit PolyAbMFF Rabbit PolyAb

Recycling autophagosome recyclers
Recycling of autophagosomal components from autolysosomes by the recycler complex

Zhou et al. Nature Cell Biology

Products cited: SNX4 Rabbit PolyAbSNX17 Rabbit PolyAb, SNX6 Rabbit PolyAbAlpha Tubulin Mouse McAb, DYNC1H1 Rabbit PolyAb


Novel role for the chaperonin subunit CCT2 in protein aggregate removal
CCT2 is an aggrephagy receptor for clearance of solid protein aggregates

Ma et al. Cell

Products cited: CCT4 Rabbit PolyAbCCT5 Rabbit PolyAbCCT6A-Specific Rabbit PolyAbCCT7 Rabbit PolyAbCCT8 Mouse McAbRB1CC1 Rabbit PolyAbGFP-Trap® Magnetic Agarose


STAR imaging microscopy confirms flexible clathrin endocytosis hypothesis
Imaging vesicle formation dynamics supports the flexible model of clathrin-mediated endocytosis

Nawara et al. Nature Communications

Products cited: Clathrin light chain A PolyAb


April featured papers
Landmark discovery of a previously unidentified protein across a wide range of neurodegenerative diseases
Homotypic fibrillization of TMEM106B across diverse neurodegenerative diseases.

Chang et al. Cell.

Products cited: TDP-43 polyclonal antibodyTMEM106B polyclonal antibodyTMEM106B monoclonal antibody

Discovering ALS risk genes using machine learning
Genome-wide identification of the genetic basis of amyotrophic lateral sclerosis.

Zhang et al. Neuron.

Products cited: TDP-43 (c-terminal) polyclonal antibody


Peroxisomes are essential for Rho-1 signalling in lipid metabolism
Modulation of the cell membrane lipid milieu by peroxisomal b-oxidation induces Rho1 signaling to trigger inflammatory responses.

Nath et al. Cell Reports.

Products cited: Peroxin 2 Polyclonal Antibody


Ancient copper homeostatic mechanism unravelled
Copper induces cell death by targeting lipoylated TCA cycle proteins.

Tsvetkov et al. Science.

Products cited: DLD polyclonal antibodyGCSH polyclonal antibodyLIAS polyclonal antibody


March featured papers
Unwinding the molecular basis of brain metastases
Cellular architecture of human brain metastases.

Gonzalez et al. Cell.

Products cited: PEG10 Polyclonal antibodyS100A6 Polyclonal antibody

An unusual role for GABA in cancer metabolism
Cancer-cell-derived GABA promotes β-catenin-mediated tumour growth and immunosuppression.

De Huang et al. Nature Cell Biology.

Products cited: GABBR2 Rabbit PolyAbBeta Actin Mouse McAbGAD65 Rabbit PolyAbGAD1 Rabbit PolyAbABAT Rabbit PolyAb.

Novel autophagy mechanism identified
A new type of ERGIC-ERES membrane contact mediated by TMED9 and SEC12 is required for autophagosome biogenesis.

Li et al. Cell Research


UNC13A exacerbates effects of TDP43 loss in ALS
TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A.

Brown et al. Nature.

Antibodies cited: TDP-43 (C-terminal) Rabbit PolyAbTDP-43 Rabbit PolyAb.

February featured papers
Finding SARS-CoV-2 vulnerabilities
Large scale discovery of coronavirus-host factor protein interaction motifs reveals SARS-CoV-2 specific mechanisms and vulnerabilities.

Kruse et al. Nature Communications.

Products cited: Myc-Trap® AgaroseGFP-Trap® AgaroseGFP-Booster ATTO488

New role for ATG9A in fatty acid metabolism
The autophagy protein ATG9A enables lipid mobilization from lipid droplets.

Mailler et al. Nature Communications.

Products cited: GFP-Trap® Magnetic AgaroseTIP47 Rabbit PolyAbATG2A Rabbit PolyAbATG2B Rabbit PolyAb

MeCP2: the great protector
MeCP2 is a microsatellite binding protein that protects CA repeats from nucleosome invasion.

Ibrahim et al. Science.

Antibodies cited: MECP2 Rabbit PolyAb

New modelling strategies for rare kidney diseases
A tissue-bioengineering strategy for modeling rare human kidney diseases in vivo.

Hernandez et al. Nature Communications

Antibodies cited: c-MYC Rabbit PolyAbHuman ENO2 ELISA KitPAX8 Rabbit PolyAb



January featured papers
Stopping the nucleosome invasion
MeCP2 is a microsatellite binding protein that protects CA repeats from nucleosome invasion. 

Ibrahim et al., 2021. Science 

Cited Proteintech’s products: MECP2 rabbit polyclonal antibody

“Balancing the control of nuclear shape” 
Regulators of tubulin polyglutamylation control nuclear shape and cilium disassembly by balancing microtubule and actin assembly. 

Wang et al., 2021. Cell Research 

Cited Proteintech’s products: KATNA1 Rabbit PolyAbSeptin 2 Mouse McAbMAP1S Rabbit PolyAbARL13B Rabbit PolyAb

“New models for kidney disease”  
A tissue-bioengineering strategy for modeling rare human kidney diseases in vivo

Hernandez et al., 2021. Nature Communications 

Cited Proteintech’s products: Human ENO2 ELISA KitPAX8 Rabbit PolyAbSIX2 Rabbit PolyAb

“A wasp-like conductor” 
STING orchestrates the crosstalk between polyunsaturated fatty acid metabolism and inflammatory responses 

Vila et al. 2021., Cell Metabolism 

Cited Proteintech’s products: FADS1 Rabbit PolyAbGAPDH Mouse MonoAb



October featured papers

''New platform for discovery and characterisation of RNA-modifying enzymes’’

Activity-based RNA-modifying enzyme probing reveals DUS3L-mediated dihydrouridylation

Dai et al., 2021 Nature chemical biology

Cited Proteintech’s products: NSUN2 Polyclonal antibodyNSUN5 Polyclonal antibody, HTF9C Polyclonal antibody  and    DUS3L Polyclonal antibody

''How cells communicate and respond to stress?’’

An mTORC1-GRASP55 signaling axis controls unconventional secretion to reshape the extracellular proteome upon stress

Nüchel et al., 2021 Molecular Cell

Cited Proteintech’s products: CHMP2A Polyclonal antibodyDYKDDDDK tag Polyclonal antibodyGOLGA2/GM130 Polyclonal antibodyGORASP2 Polyclonal antibodyGORASP2 Monoclonal antibodyTMEM59 Polyclonal antibodyTMF1-Specific Polyclonal antibody  and    p115, USO1 Polyclonal antibody

''Severity of COVID-19 is guided by variations in interferon genes’’

A prenylated dsRNA sensor protects against severe COVID-19

Wickenhagen et al., 2021 Science

Cited Proteintech’s products: OAS1 Polyclonal antibodyOAS2 Polyclonal antibody  and    OAS3 Polyclonal antibody

''APPLE as a target for cancer treatment’’

The oncomicropeptide APPLE promotes hematopoietic malignancy by enhancing translation initiation

Sun et al., 2021 Molecular Cell

Cited Proteintech’s products: PDI Polyclonal antibodyEIF4G1 Polyclonal antibodyGABARAP Polyclonal antibodyKRAS Polyclonal antibodyHRP-conjugated 6*His, His-Tag Monoclonal antibody  and    GAPDH Polyclonal antibody

September featured papers

‘'Liver origin problem solved’'

Quantitative lineage analysis identifies a hepato-pancreato-biliary progenitor niche

Willow et al., 2021 Nature

Cited Proteintech's products: ARL13B Polyclonal antibody and ChromoTek RFP Monoclonal antibody (5F8)

‘'Kidney disease risk genes found to regulate iron-dependent apoptosis’'

A single genetic locus controls both expression of DPEP1/CHMP1A and kidney disease development via ferroptosis

Guan et al., 2021 Nature Communications

Cited Proteintech's products: DPEP1 Polyclonal antibodyCHMP1A Polyclonal antibody and GAPDH Monoclonal antibody

‘'New oncogene identified for potential treatment of hepatocellular carcinomas''

Genomic gain of RRS1 promotes hepatocellular carcinoma through reducing the RPL11-MDM2-p53 signaling

Cao et al., 2021 Science Advances

Cited Proteintech's products: RRS1 Polyclonal antibody, P53 Polyclonal antibody, P21 Polyclonal antibody, BCL2 Polyclonal antibody, PUMA Polyclonal antibody, RPL5 Polyclonal antibody, RPL11 Polyclonal antibody, HUWE1 Polyclonal antibody, RCHY1 Monoclonal antibody, B23/NPM1 Monoclonal antibodyLamin B1 Polyclonal antibody, ubiquitin Polyclonal antibody and MYC-tag Polyclonal antibody

‘'TAX and cargo receptors regulate protein aggregates disposal’' 

Reconstitution defines the roles of p62, NBR1 and TAX1BP1 in ubiquitin condensate formation and autophagy initiation

Turco et al., 2021 Nature Communications

Cited Proteintech's products: ChromoTek RFP Monoclonal antibody (6G6),  ChromoTek GFP-Trap® Magnetic Agarose and ChromoTek RFP-Trap Agarose

Publication Spotlight highlights the new and exciting discoveries citing Proteintech antibodies published in scientific journals across the globe.

100,000 success stories and counting. What matters to Proteintech is the success of its antibodies in the hands of scientists - the people who make the discoveries that change and explain the world around us. In reaching 100,000 citations of Proteintech antibodies, our thanks go out to the talented researchers who made this milestone possible by using Proteintech antibodies in their work.

August featured paper

Cousin et al. Nature Genetics

‘Pathogenic SPTBN1 variants cause an autosomal dominant neurodevelopmental syndrome’

Ubiquitously expressed polypeptides that bind membrane lipids are known as spectrins; which bind ankyrins to line the cellular plasma membrane. The Spectrin meshwork is formed by heterodimeric α-spectrin and β-spectrin units. Mammalian neurons contain a wide range of spectrins including αII-spectrin and βI-V spectrins. Spectrins with ankyrins position and stabilise cellular adhesion molecules, membrane transporters, ion channels and scaffolding proteins. Previously, autosomal dominant variants in βIII-spectrin (SPTBN2) were identified and associated with late-onset spinocerebellar ataxia type 5, while autosomal recessive variants were found to be linked with childhood ataxia and intellectual disability. In the recent publication (PMID:34211179) Cousin et al. identified heterozygous variants of SPTBN1 affecting βII-spectrin stability, contributing to the neurodevelopmental disorder development.

The authors performed whole-exome sequencing (WES) on a cohort of 29 individuals from 28 different families with heterozygous SPRBN1 variants. WES identified 28 unique variants, of which: 22 were missense, three nonsense and three canonical splice-site variants. SPTBN1 variants were found to contribute to various neurological and behavioural changes causing neurodevelopmental syndrome. Seventeen unique SPTBN1 variants were classified as pathogenic, nine as likely pathogenic, and the two remaining of uncertain significance. Subsequently, a subset of SPTBN1 variants was introduced in GFP-targeted human βII-spectrin to assess the pathogenic mechanism of SPTBN1 variants. This experiment revealed that SPTBN1 variants in βII-spectrin cause changes to cytoskeleton structure and dynamics altering cellular morphology, and in turn causing disruptions in neuronal architecture which contribute to SPTBN1-associated syndrome. In turn, the effects of βII-spectrin haploinsufficiency and deficiency were assessed in vivo. βII-spectrin knockout (KO) mice showed that βII-spectrin loss of function can reduce neural connectivity, affecting global development and behaviour, and contributing to development of social behaviour impairments and autistic features which were observed with lesser severity in haploinsufficient animals.

This study reported de novo SPTBN1 variants that affect βII-spectrin stability through disruption of cytoskeleton organisation and dynamics, together with disrupted binding of key molecular partners. Collectively, these results revealed that SPTBN1 variants are linked to the development of neurodevelopmental disorder, intellectual disability, and behavioural comorbidities.

Six Proteintech antibodies were used in this study for Western Blot and Immunoprecipitation: GFP tag Monoclonal (66002-1-Ig), GFP tag Polyclonal (50430-2-AP), HA tag Polyclonal (51064-2-AP), Alpha-tubulin Monoclonal (66031-1-Ig) and 6xHis tag Monoclonal (66005-1-Ig).

Western blot of eGFP-tagged fusion protein with GFP tag Polyclonal antibody at various dilutions

Immunoprecipitation experiment of transfected HEK-293 using HA tag Polyclonal antibody

About the corresponding authors: Dr Margot A. Cousin is a Research Associate at Mayo Clinic in Rochester, USA; Dr Damaris N. Lorenzo is an Assistant Professor at the University of North Carolina where she runs a laboratory which studies ankyrins, spectrins and their partners in the aspects of cellular homeostasis and human disease.

July featured papers

“Super cilia signalling”

Ciliopathy protein HYLS1 coordinates the biogenesis and signaling of primary cilia by activating the ciliary lipid kinase PIPKIγ

Antibodies cited: IGFBP4, IFT88, IFT140, NPHP4TULP3, KIF7, RPGRIP1L, GPR161, INPP5E, MKS1, SCLT1, TCTN1, FBF1, ARL13B, HA tag

“Newly discovered Leucine sensor may promote lung tumour development”

SAR1B senses leucine levels to regulate mTORC1 signalling

Chen et al. Nature

Cited Antibodies: MYOD1, CKM-Specific , MYL1 , SESN1 Sestrin 2 , WDR24 , SAR1B , SAR1A , TMEM173/STING.

“Calcium signaling is helped by KRAP”

KRAP tethers IP 3 receptors to actin and licenses them to evoke cytosolic Ca 2+ signals

Thillaiapan et al. Nature Communication

Cited Antibodies: KRAP/SSFA2 Polyclonal antibody, ChromoTek GFP-Booster ATTO488


“Aging associated changes in the nucleocytoplasmic transport pathway is linked to ALS”

Interactions between ALS-linked FUS and nucleoporins are associated with defects in the nucleocytoplasmic transport pathway

Lin et al. Nature Neuroscience

Cited Antibodies: POM121 Polyclonal antibody, FUS/TLS Polyclonal antibody

June featured papers

“Heart failure has met it’s MARK(4)”

MARK4 controls ischaemic heart failure through microtubule detyrosination.

Yu et al. Nature

Cited Antibodies: TTL Polyclonal antibody

“SARS-CoV-2 has a nose for cilia”

Nasal ciliated cells are primary targets for SARS-CoV-2 replication in early stage of COVID-19

Ahn et al. Nature

Cited Antibodies: Acetylated Tubulin(Lys40) Monoclonal antibody

“Stress collides with ribosomes to activate cGAS”

Translation stress and collided ribosomes are co-activators of cGAS

Wan et al. Molecular Cell

Cited Antibodies: ASCC1 Polyclonal antibody, IFIT2 Polyclonal antibody, GFP-Trap Magnetic Agarose

“Metformin attenuates pulmonary inflammation by SARS-CoV-2”

Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation

Xian et al. Immunity

Cited Antibodies: NFATC3 Polyclonal antibody, NDUFS4 Polyclonal antibody

February featured papers

“Nice to METTL3 you” 

METTL3 regulates heterochromatin in mouse embryonic stem cells. 

Xu et al. Nature 



“Mitochondrial stabilizers” 

C9orf72 regulates energy homeostasis by stabilizing mitochondrial complex I assembly 

Wang et al. Cell Metabolism 

Cited Antibodies: C9orf72Tim23YME1L1  

“Autophagy cargo selector” 

Systematically defining selective autophagy receptor-specific cargo using autophagosome content profiling 

Zellner et al. Molecular Cell 


“Plant perception” 

Perception of a divergent family of phytocytokines by the Arabidopsis receptor kinase MIK2. 

Rhodes et al. Nature Communications 

Cited Products: ChromoTek RFP-Trap® AgaroseChromoTek GFP-Trap® Agarose  

January featured papers

“RNA handcuffs devious retroviruses” 

m6A RNA methylation regulates the fate of endogenous retroviruses 

Chekmicki et al. Nature 

Cited Antibodies: YTHDF1YTHDF2WTAP 

“Flava Flavirus” You know the time!” 

TMEM41B Is a Pan-flavivirus Host Factor 

Heinrich Hoffman et al. Cell. 

Cited antibodies: TMEM41A 

“Like father, like son 

Comparative host-coronavirus protein interaction networks reveal pan-viral disease mechanisms. 

Gordon et al. Science 

Cited Antibodies: TOM20 

“Nowhere to run, nowhere to hide” 

Targeting Endogenous K-RAS for Degradation through the Affinity-Directed Protein Missile System 

Roth et al. Cell Chemical Biology 

Cited Antibodies: NRASHRAS, KRAS-2A, KRAS-2B 

December featured papers
“Closed for a private TDP43 event”

HSP70 chaperones RNA-free TDP43 into anisotropic intranuclear liquid spherical shells

Yu et al. Science.

Cited antibodies: TDP-43 (C-Terminal)

 “Metastatic information highway”

A metastasis map of human cancer cell lines.

Jin et al. Nature.

Cited antibodies: SREBF1

 “Viral prison break”

Decreased Expression of the Host Long-Noncoding RNA-GM Facilitates Viral Escape by Inhibiting the Kinase activity TBK1 via S-glutathionylation.

Wang et al. Immunity

Cited antibodies: GSTM1, MAVS, HRP-6*His-Tag, Beta Actin.

 “Traffic cops of the golgi”

Oleate-induced aggregation of LC3 at the trans-Golgi network is linked to a protein trafficking blockade.

Cerrato et al. Cell Death and Differentiation

Cited antibodies: TGN46

November featured papers
Pesky persistence to BRAF/MEK inhibitors 

Melanoma Persister Cells Are Tolerant to BRAF/MEK Inhibitors via ACOX1-Mediated Fatty Acid Oxidation 

Shen et al. Cell Reports 

Cited antibodies: CPT1AACOX1PPARαPGC1a 

“Giving the DNA surgeon some room to operate” 

USP52 regulates DNA end resection and chemosensitivity through removing inhibitory ubiquitination from CtIP. 

Gao et al. Nature Communications 

Cited antibodies: DMT1KRASCD44PCCAGADPH 

“Super Genomics finds pancreatic cancer Kryptonite” 

Functional Genomics Identifies Metabolic Vulnerabilities in Pancreatic Cancer 

Biancur et al. Cell Metabolism 

Cited antibodies: FDFT1 

Not included in Miss Manners etiquette book 

Identification of Required Host Factors for SARS-CoV-2 Infection in Human Cells. 

Daniloski et al. Cell 

Cited antibodies: ATP6V1ACCDC22 

October featured papers

Cytoplasmic control of intranuclear polarity by human cytomegalovirus

Procter et al. Nature 

Cited antibodies: Emerin 

“Does this work for 2020 too?"

A Cellular Mechanism to Detect and Alleviate Reductive Stress 

Manford et al. Cell 

Cited antibodies: FEM1B

“You scratch my back and I’ll scratch yours” 

Reciprocal Interaction between Vascular Filopodia and Neural Stem Cells Shapes Neurogenesis in the Ventral Telencephalon 

Di Marco et al. Cell Reports 

Cited antibodies: VEGF-A 

“The most cited paper by tooth fairies” 

Dental cell type atlas reveals stem and differentiated cell types in mouse and human teeth 

Krivanek et al. Nature Communications 

Cited antibodies: Smooth muscle actin 

September featured papers
“Protein buddy system”

Structural basis for dimerization quality control.

Mena et al. Nature

Cited antibodies: PDCD6

“Schwann cells to the rescue”

A glycolytic shift in Schwann cells supports injured axons

Babetto et al. Nature Neuroscience

Cited antibodies: RICTOR, Raptor, OGDH, IDH3A, Citrate synthase, LDHB, PGK1, PFKM, GPI

“Cancer slugger”

Glutamine depletion regulates Slug to promote EMT and metastasis in pancreatic cancer.

Recouvreux et al. J Exp Med

Cited antibodies: Sestrin 2, ASNS

“VAMPing up ER-phagy”

CALCOCO1 acts with VAMP-associated proteins to mediate ER-phagy.

Nthiga et al. EMBO J

Cited antibodies: CKAP4, FAM134B, VAPB, VAPA.

August featured papers

Download the printer friendly version here

“It’s NRF2 or Nothin”

Activation of NRF2 ameliorates oxidative stress and cystogenesis in autosomal kidney disease.

Lu et al. Sci Trans Med

Cited antibodies: alpha-tubulin,   KEAP1,   NQO1

GALC it up

Neuron Macrophages Expressing GALC Improve Peripheral Krabbe Disease by a Mechanism Independent of Cross-Correction

Weinstock  et al. Neuron

Cited antibodies: CD206,    OLIG2,   PMP2

Sympathy for the adipose tissue

A leptin-BDNF pathway regulating sympatheticinnervation of adipose tissue

Wang  et al. Nature

Cited antibodies:   UCHL1
MegaDalton Protein to the rescue

Naked mole-rat very-high-molecular mass hyaluronan exhibits superior cytoprotective properties.

Takasugi  et al. Nat. Comm

Cited antibodies:  P53,   CD44

The Pearly Cilia

TALPID3 and ANKRD26 selectively orchestrate FBF1 localization and cilia gating

Gates Yan  et al. Nat. Comm

Cited antibodies:   ARL13B ,  FBF1 ,   GAPDH ,   IFT140 ,   KIAA0586,  NKIRAS2SCLT1TCTN1





Lu et al.

Science Translational Medicine

Activation of NRF2 ameliorates oxidative stress and cystogenesis in autosomal dominant polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is a deadly genetic disorder caused by mutations in PKD1/2 genes. It is characterized by renal cysts that fill with fluid, leading to kidney failure. Current therapeutic approaches provide only a few years of life after diagnosis, with kidney transplants being the most effective current treatment. In a recent study (PMID: 32727915), Yi Lu and colleagues discover a potential pharmaceutical target for this disease.

To find therapeutic targets for ADPKD, Lu and colleagues compared the proteomic signatures of kidneys from genetic ADPKD model (Pkd1-/-) and wild-type mice, and found that proteins involved in mitochondrial function were downregulated in ADPKD kidneys. Investigating this further, it was discovered that reactive oxidative species (ROS) levels were high in these tissues and that increasing ROS levels correlated with disease progression in patients. Consequently, they examined whether a key transcription factor in ROS maintenance, NRF2, may be responsible. Not only were NRF2 levels lower in ADPKD kidneys, but all its gene targets were also decreased. Knocking this gene out in a genetic ADPKD mouse model (Pkd1−/−;Nrf2−/−) increased disease severity. Consistent with NRF2 playing a protective role, increasing NRF2 activity by pharmacological inhibition of its two negative regulators improved the health of ADPKD mice. To understand the mechanism, the authors next examined the genomic effects of inducing NRF2 activity in the ADPKD 9-12 cell line. Using ChIP-SEQ, they found that NRF2 was bound to enhancers to the active histone markers H3K4Me1 and H3K27ac, suggesting increased target gene transcription. Comparing ChIP-SEQ data of ADPKD cells with and without pharmacological downregulation of NRF2 inhibitors, it was revealed that histone acetyltransferase P300 has a similar footprint to NRF2, suggesting NRF2 recruits P300 to add activating markers to its enhancers. Further supporting this, the enhancer targets all had increased activity in the treatment condition. Diving deeper into the enhancer mechanism, the authors tested the possibility that NRF2 forms a phase-separated complex with MED1 of the transcription machinery to promote transcription. Using an in vitro droplet formation assay, they showed that NRF2 can form phase-separated compartments and that MED1 can be included in these compartments. Consistent with this hypothesis, ChIP-SEQ revealed that NRF2 and MED1 occupy the same genomic regions. Overall, the group’s work suggests that loss of NRF2 is critical to the progression of ADPKD and that targeting its regulators may be an effective therapeutic strategy.

Three Proteintech antibodies were used in this study for Western blot: KEAP1 (10503-2-AP), NQO1 (11451-1-AP), and alpha-tubulin (11224-1-AP).

Western blot analysis of HEK293 cells that were untransfected (Lane 1) and transfected with si-KEAP1 vector (Lane 2) using KEAP1 antibody (10503-2-AP).

About the corresponding author, Dr. Yupeng Chen: Yupeng Chen is a professor in the Collaborative Innovation Center of Tianjin for Medical Epigenetics at Tianjin Medical University in China. His laboratory focuses on kidney diseases and epigenetics.


Huang et al.


Origins and Proliferative States of Human Oligodendrocyte Precursor Cells

Much of human evolution can be attributed to the increase in size and complexity of the cerebral cortex. Cerebral white matter is developed from myelinating oligodendrocytes, arising from the differentiation of oligodendrocyte precursor cells (OPCs). A key challenge in this field is to understand their development in humans, as much previous work was performed in rodents, which have vastly decreased white matter. Humans make use of an enlarged cortical germinal zone, the outer subventricular zone (OSVZ), which is populated with outer radial glia (oRG) and progenitors for OPCs. How human OPC production is developed from this zone is poorly understood, and understanding this process is key to finding new treatments to traumatic brain injuries in addition to deepening our understanding of white matter expansion.

In this work (PMID: 32679030), Huang and colleagues studied the transcriptional profile of embryonic human brain tissue samples using unbiased capture in combination with immunopanning to identify high quality cells with classic OPC markers. Their analysis revealed a subset of cells containing markers for both neural progenitor cell (NPC) and OPC lineage, suggesting a transitional pre-OPC stage. They found over 10% of OPCs express low levels of transcriptional markers for both OPCs and NPCs, which, along with their immature morphology, suggested the role of these cells is a transitional intermediate between OPCs and NPCs. They then tested whether potential pre-OPC cells were capable of becoming OPCs in vitro. After 7 days in culture, around half of the cells demonstrated a reduction in progenitor markers and an upregulation in mature OPC markers such as OLIG2 and PDGFRA, indicating that these progenitors can generate OPCs. They then investigated the origin of the pre-OPC cells. One candidate was neurogenic oRGs, which play a role in gray matter expansion in humans, because the transcriptional profile of the pre-OPC cluster also contained oRG gene markers, such as HOPX. Furthermore, immunohistochemical analysis revealed that a small percentage of oRGs and pre-OPCs in the OSVZ both expressed HOPX. To test whether HOPX-expressing oRGs could generate OPCs, these cells were isolated and cultured in vitro. By day 10, roughly 17% of cells expressed mature OPC markers (OLIG2 and PDGFRA), suggesting that oRGs can produce OPCs and thus may be an additional source of OPCs in the developing human brain. Time-lapse imaging and GFP labeling showed that pre-OPCs had mitotic somal translocation during division, similar to oRGs, and regrew processes similar to OPCs. The authors also observed that OPCs divided symmetrically and frequently, in comparison to mouse embryonic OPCs, which divide only once in 5 days. These findings indicate the properties, derivation, and proliferation of OPCs from oRGs in the developing human brain, an important part of white matter expansion.

Proteintech’s HOPX antibody (11419-1-AP) was used in this study as a marker of oRG cells, utilizing immunofluorescence to track the development of oRGs to pre-OPCs in vitro.

WB analysis of mouse lung tissue using 11419-1-AP

Mouse lung tissue were subjected to SDS PAGE followed by western blot with 11419-1-AP (HOPX antibody) at dilution of 1:300 incubated at room temperature for 1.5 hours.

About the corresponding author:  Arnold Kriegstein is a Professor of Neurology at the University of California, San Francisco. His work focuses on the embryonic development of neural cells.


Qian et al.


Reversing a model of Parkinson’s disease with in situ converted nigral neurons 

Parkinson’s disease is a neurodegenerative disorder affecting motor function. The major neurons affected are dopaminergic neurons in the substantia nigra pars compacta in the midbrain. A potential therapeutic approach for this disease is regenerative medicine. Previous work had demonstrated that repressing transcription factors PTB and nPTB can convert human fibroblasts to neurons. In this work (PMID: 32581380), Qian et al. extend this insight to astrocytes, demonstrating that targeting a single protein – PTB – can efficiently convert astrocytes to dopaminergic neurons. Remarkably, these converted neurons restored motor function in a Parkinson’s mouse model, paving the way for in vivo regenerative medicine.

Due to the plasticity of astrocytes, Qian and colleagues hypothesized that astrocytes, like fibroblasts, could be transcriptionally reprogrammed into neurons. Comparing the transcriptional programming between neurons, astrocytes, and fibroblasts, they found that the necessary nPTB repression loop was already in place for astrocytes and that only the PTB repression loop needed to be implemented to facilitate conversion. To test whether PTB knockdown was sufficient for neural conversion, Qian and colleagues delivered a lentiviral shRNA construct to midbrain astrocytes in mice. The morphology, marker expression, and function of the converted astrocytes were consistent with dopaminergic neurons in the targeted region, thus validating their conversion. Additionally, the axons of the converted astrocytes targeted the appropriate brain subregions. Qian and colleagues then tested the ability of converted astrocytes to restore function in a Parkinson’s mouse model. Lentiviral delivery of PTB shRNA resulted in a partial restoration of the number of dopaminergic neurons. Furthermore, dopamine biogenesis and activity-induced release of the converted astrocytes were nearly similar to controls, indicating their potential to sufficiently replace lost neurons. To test the functionality of these converted neurons in vivo, mice were treated with PTB shRNA and they performed at a similar level as control mice in motor-skills tests. Lastly, using a chemogenetic approach targeting dopaminergic neurons, they showed that the converted astrocytes were responsible for the effects. Since lentiviral delivery is not clinically viable, Qian and colleagues then tested whether injection of a more practical therapy, anti-sense oligos, could achieve the same results. Marker expression and behavioral testing suggested that this approach has similar efficacy to lentiviral delivery. Though proof-of-concept, these results suggest an elegant genetic method for limiting the effects of Parkinson’s disease, and could revolutionize the treatment of this disease moving forward.

Proteintech antibodies were used in this study. VMAT2 (20873-1-AP), DAT (22524-1-AP), ALDH1L1 (17390-1-AP), Calbindin D28K (14479-1-AP), OTX2 (13497-1-AP), SOX6 (14010-1-AP), and S100b (15146-1-AP) were used as dopaminergic neuron markers. Cux1 (11733-1-AP) was used as a cortical neuron marker and beta-actin (66009-1-IG) was used as a loading control.

IF staining of mouse brain tissue using 22524-1-AP

Immunofluorescent analysis of fixed mouse brain tissue using 22524-1-AP (1:50, green) and DAPI (blue). About the corresponding author, Xiang-Dong Fu, PhD: Dr. Fu is a Distinguished Professor of Cellular and Molecular Medicine at the University of California, San Diego. His lab focuses on RNA regulation and fate determination.


Ying et al.

Nature Communications

Activation of GCN2/ATF4 signals in amygdala PKC-δ neurons promotes WAT browning under leucine deprivation

Recently, the conversion of white adipose tissue (WAT) into a high energy consuming state similar to brown adipose tissue has received increased attention due to its therapeutic potential to combat obesity and metabolic disorders. WAT browning increases the metabolic capacity of WAT cells by promoting the use of free fatty acids as fuel, occurring in response to prolonged cold exposure, intermittent fasting, and low-protein/high-carbohydrate diets. Specifically, branched chain amino acids such as leucine and valine are highly important in metabolic pathways regulating lipid metabolism and glucose utilization. Distinct neurons in the hypothalamus in the brain, a key area for processing metabolic signals, are primarily responsible for the central control of processes that influence WAT browning. Recently, certain neurons in the amygdala have been shown to influence certain metabolic processes, an area not traditionally known for metabolic functions.

Yuan and colleagues published a recent paper in Nature Communications, describing the role of leucine deprivation in the regulation of WAT browning. They discovered that dietary leucine deprivation induced WAT browning, but that this induction can be blocked by inhibiting protein kinase c-δ (PKC-δ) neurons in the amygdala, indicating the high-level involvement of these neurons in this process. The authors went on to describe a possible mechanism for this phenomenon through general control nonderepressible 2 (GCN2), a neuronal amino acid sensor in the amygdala, and its downstream effector, activating transcription factor 4 (ATF4). Specifically, deleting GCN2 from PKC-δ amygdala neurons reduced the amount of WAT browning seen following leucine deprivation. Supporting this finding, they showed that blocking activation of ATF4 in these neurons was also able to decrease markers of WAT browning. These results highlight a novel role of central amino acid sensing through GCN2 and its interactions with ATF4 in the amygdala, shedding light on possible dietary interventions to induce WAT browning and thus providing novel pathways to help treat metabolic disease.

Proteintech’s ATF4 antibody (10835-1-AP) was used in this study to confirm ATF4 knockdown in PKC-δ in amygdala neurons. This antibody has been cited 125 times and validated in WB, IP, IHC, IF, FC, and ELISA.

WB analysis of A431 cells using 10835-1-AP

A431 cells were subjected to SDS PAGE followed by western blot with 10835-1-AP at a dilution of 1:500 and incubated at room temperature.

About the corresponding author:

Feifan Guo. Professor Guo is a professor at the Shanghai Institute of Nutrition and Health, and her work focuses on the molecular mechanisms underlying nutrition-related metabolic diseases. 


Zhao et al.


Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate

Obesity is a growing problem across the world due, in part, to increased fructose consumption. It is well known that fructose causes the liver to produce lipids in a process called de novo lipogenesis (DNL), so a key enzyme in converting fructose to acetyl-CoA, ACLY, has been an attractive therapeutic target. However, in a recent Nature paper (PMID: 32214246), Zhao and colleagues demonstrate that ACLY is not involved in fructose-induced DNL and that microbiota metabolize dietary fructose into acetate to fuel DNL in the liver.

To investigate the role of ACLY in hepatic DNL, Zhao and colleagues assayed the response of ACLY KO mice to high fructose consumption compared to wild-type controls. Surprisingly, both KO and control mice showed the same DNL response, suggesting that this process does not require ACLY. To find clues to this alternative route to DNL, they investigated the transcriptional response to fructose. They found that ACSS2, which converts acetate to acetyl-CoA, significantly increases upon fructose consumption. This result raised the possibility that acetate may be playing a role. Consistent with acetate being the favored substrate for fructose-induced DNL, hepatocytes incorporate acetate more readily than fructose in DNL. In vivo, DNL intermediates appear much later than fructolytic intermediates and increase significantly after acetate appears in the portal blood. A possible source of acetate is the gut microbiota. To test this, Zhao and colleagues performed an oral gavage of radioactive-labeled fructose to wild-type mice with and without antibiotic treatment. Though fructolytic intermediates were unchanged between the two groups, antibiotic-treated mice had a lower DNL response. Furthermore, an oral gavage of fructose and radioactive-labeled acetate resulted in similar DNL responses between groups. Interestingly, the transcriptional response to fructose was independent of antibiotic treatment. Overall, Zhao et al.’s study suggests an interplay between the microbiota and organs in DNL, and casts doubt on the potential therapeutic efficacy of ACLY inhibitors for obesity and non-alcoholic fatty liver disease.

Proteintech’s ACLY antibody (15421-1-AP) was used in this study to confirm their knockout mouse model and show ACLY induction after fructose consumption. This antibody has been validated in WB, IP, IHC, IF, and FC.

WB analysis of L02 cells using 15421-1-AP

Various lysates were subjected to SDS-PAGE followed by Western blot with ACLY antibody (15421-1-AP) at 1:2000 dilution and incubated at room temperature for 1.5 hours.

About the corresponding author, Kathryn E. Wellen:

Dr. Wellen is an associate professor of Cancer Biology at the University of Pennsylvania Perelman School of Medicine. Her research focus is the biochemistry of cancer and metabolic disease.   


Hui et al.

Lancet Respiratory Medicine

Tropism, Replication Competence, and Innate Immune Responses of the Coronavirus SARS-CoV-2 in Human Respiratory Tract and Conjunctiva: An Analysis in Ex-Vivo and In-Vitro Cultures

A key part of mitigating the risk of infection by the novel coronavirus is understanding how it enters the body and which parts of each organ it infects. In a recent Lancet Respiratory Medicine article (PMID: 32386571), Hui and colleagues explored the ability of SARS-CoV-2 to infect different tissues.

To investigate organ tropism of SARS-CoV-2, Hui et al. first generated ex vivo cultures of bronchus, ocular conjunctiva, and lung tissues. They then infected them with either SARS-CoV-2, SARS-CoV, H1N1, or MERS-CoV and assessed infection after 4 days using immunohistochemical staining of viral components. All the tissues showed viral staining, indicating infection. Next, Hui and colleagues compared the replication rate of the different viruses in their ex vivo cultures. In comparison to MERS-CoV, SARS-CoV-2 replication was nearly identical in the bronchus, and less than MERS-CoV in the lung. In comparison to SARS-CoV, SARS-CoV-2 replication was higher in the bronchus and similar in the lung and ocular conjunctiva. Interestingly, proinflammatory cytokines were at lower levels after infection with SARS-CoV-2 than H1N1, MERS-CoV, and SARS-CoV. Overall, the study suggests that the bronchus, lung, and ocular conjunctiva are viable entries for SARS-CoV-2 infection and this may help inform health policies.

Proteintech’s CC10 antibody (10490-1-AP) was used to label club cells in their bronchus ex vivo cultures. This antibody has been validated for use in WB, IHC, and IF.

 IHC staining of mouse lung tissue using 10490-1-AP

Immunohistochemical analysis of mouse lung tissue using CC10 antibody (10490-1-AP, 1:200).

About the corresponding author, Michael Chan:

Michael Chan, PhD is an associate professor in the School of Public Health at the University of Hong Kong. His research focus is on coronavirus and influenza pathogenesis. 


Schworer et al.


Proline biosynthesis is a vent for TGFB-induced mitochondrial redox stress

Underneath a wound as minor as a simple paper cut is a complex coordinated response of signaling and protein production. One key growth factor in wound healing is TGFB. This signal causes fibroblasts to generate collagens, essential extracellular matrix components. Collagens are enormous proteins rich in proline and glycine, so TGFB signaling needs to reprogram metabolism to enable production. In a recent EMBO paper (PMID: 32134147), Schworer et al. show that TGFB signaling enables fibroblasts for collagen production by rapidly increasing the rate of oxidative phosphorylation, setting off a cascade of events. The high activity of the TCA cycle creates excessive redox potential, which in turn promotes proline biosynthesis. The accumulation of this amino acid then enables the production of proline-rich collagens.   

To understand the metabolic shift during wound healing, Schworer and colleagues first examined the metabolic state of NIH-3T3 fibroblasts stimulated with TGFB. Measuring ATP and metabolite levels, they found that TGFB increases glutamine consumption, protein translation, TCA cycle activity, and oxidative phosphorylation. Consistent with this growth factor stimulating collagen deposition, TGFB-conditioned fibroblasts elevated synthesis of collagen’s major amino acids: proline and glycine. The link between TGFB and proline levels is not well-characterized, so Schworer and colleagues investigated whether proline biosynthesis – a process that consumes NADH and NADPH – is a redox vent from elevated TCA cycle activity during TGFB stimulation. To test this, they ectopically expressed NADH and NADPH oxidases to act as competing redox sinks and found that these conditions eliminated proline biosynthesis. Consistent with their hypothesis, disabling proline biosynthesis by genetically deleting key enzymes resulted in ROS accumulation. Schworer et al.’s work suggests a novel link between signal transduction and metabolism to increase collagen production in fibroblasts and may provide insight into fibrotic diseases. 

Four Proteintech antibodies were used in this study. SLC25A1 antibody (15235-1-AP) was used to verify gene knockout in an experiment assessing TGFB’s effect on ROS production. PYCR1 (20962-1-AP) and PYCR2 (17146-1-AP) antibodies were used to show that TGFB upregulates the proline biosynthetic pathway. Lastly, using the Collagen IV (55131-1-AP) antibody, the authors demonstrated TGFB’s potent effect on collagen IV deposition.

IF staining of HepG2 cells using 15235-1-AP

Immunofluorescent analysis of HepG2 cells using 15235-1-AP (SLC25A1 antibody, 1:50) and Alexa Fluor488-conjugated AffiniPure goat anti-rabbit IgG(H+L) with nuclear DNA stained by DAPI.

About the corresponding author, Craig Thompson:

Dr. Thompson is the current president of the Memorial Sloan Kettering Cancer Center. His work focuses on cancer metabolism and immunology. He has over 30 patents and has founded several biotechnology companies.


Zhang et al. 


A Translocation Pathway for Vesicle-Mediated Unconventional Protein Secretion  

Like any bustling metropolis, the cell needs many on-ramps onto the highway to exit town. The major on-ramp for secreted proteins is through recognition of a specific amino acid motif by a signal recognition particle and translocation into the ER. However, some proteins lacking this motif are secreted, such as IL-1B, suggesting alternative routes of transport. In a recent Cell paper (PMID: 32272059), Zhang et al. uncover the mechanism behind the unconventional secretion of IL-1B.

To identify the machinery involved in vesicular translocation of IL-1B, Zhang and colleagues created a “trap” for protein channels. Since IL-1B’s vesicular translocation had previously been shown to be dependent on its own unfolding, they added a DHFR tag that can be maintained in the folded state in the presence of aminopterin. The idea is that the IL-1B-DHFR recombinant protein plus aminopterin would become trapped in the pore and mass spectrometry of the cross-linked complex would allow for the identification of the translocation machinery. Their assay revealed TMED10 as a potential component, which was validated using genetic manipulation, usage of different cell lines, and a mouse model. To understand the interaction between TMED10 and IL-1B, they performed a series of co-immunoprecipitation experiments with different TMED10 mutants. This analysis suggested that IL-1B directly interacts with TMED10’s C-terminal domain for translocation. They then looked at whether TMED10 is involved in the unconventional secretion of other proteins. Consistent with a broad role, genetic knockdown of TMED10 decreased secretion of many interleukin family members and other proteins. To understand the mechanism of TMED10-mediated translocation, Zhang and colleagues created an in vitro proteoliposome protection assay. Through this system, they determined that TMED10 requires unfolding of the cargo target and is sufficient for driving translocation. Moving back into a cellular system to view the events after translocation, they determined that TMED10-bearing vesicles interface with the ER-Golgi intermediate compartment using immunofluorescence and confirmed that these vesicles contain IL-1B using a split-GFP construct. Overall, their work suggests that TMED10 is an essential translocator for the unconventional secretion of IL-1B and other proteins.

Three Proteintech Antibodies were used in this study: GRP94 (14700-1-AP), TMED9 (21620-1-AP), and TMED10 (15199-1-AP). All were used for Western blotting, while the TMED10 antibody was used as the major antibody for determining TMED10 levels and localization throughout the study. The authors also validated it in KO cell lines (Figure 1 in PMID: 32272059). 

Various lysates were subjected to SDS-PAGE followed by Western blotting with 15199-1-AP (TMED10 antibody, 1:2500). 

About the corresponding author: 

Dr. Liang Ge is an assistant professor at Tsinghua University in Beijing, China. His research focuses on understanding the mechanisms behind unconventional secretion and organelle interaction.


Li et al.

Nature  Metabolism

Myc-mediated SDHA acetylation triggers epigenetic regulation of gene expression and tumorigenesis

In a recent paper, Li and colleagues examined the role of transcription factor cMyc, deregulated in many cancers, on the epigenetic regulation of gene expression. Using mass spectroscopy, western blotting, and immunoprecipitation in an expression-inducible cell system, they discovered that cMyc is responsible for the lysine acetylation of many mitochondrial proteins, including succinate dehydrogenase complex subunit A (SDHA), an enzyme in the tricarboxylic (TCA) cycle. cMyc causes proteasome-dependent degradation of SIRT3 deacetylase, which leads to increased acetylation of SDHA at Lys335 by cMyc, which in turn decreases the enzymatic activity of SDH. As a consequence, increased levels of succinate lead to changes in gene expression and increased histone methylation (H3K4me3), as detected by ChIP-seq, due to lower activity of KDM5A demethylase. Using mouse xenograft experiments and analysis of human cancer slices, Li and colleagues demonstrated that the tumor progression of cancers with deregulated Myc is at least in part mediated by higher SDHA acetylation levels uncovering an important mechanism of the epigenetic regulation of cellular metabolism in cancer by Myc.

About the corresponding author: 

Dr Ping Gao works at the University of Science and Technology of China in Hefei (China) and focuses on studying metabolism in cancer and stem cells with a particular interest in the regulation of metabolism by the cMyc oncogene. 

ACAT1 antibody SDHA antibody
 WB analysis of MCF-7 cells using 16215-1-AP IHC staining of human kidney tissue using 14865-1-AP 
WB result of ACAT1 antibody (16215-1-AP; 1:1000; incubated at room temperature for 1.5 hours) with sh-Control and sh-ACAT1 transfected MCF-7 cells Immunohistochemical analysis of paraffin-embedded human kidney tissue slide using 14865-1-AP (SDHA Antibody) at a dilution of 1:50 (under 40x lens).


Fessler et al.


A pathway coordinated by DELE1 relays mitochondrial stress to the cytosol

Monitoring the stress of the mitochondria is critical to eukaryotic cell survival. How that stress is communicated to the rest of the cell and initiates the integrated stress response is unknown. Writing in Nature (PMID: 32132706), Fessler and colleagues suggest that mitochondrial stress triggers the cleavage and subsequent release of mitochondrial DELE1 into the cytosol where it binds to HRI to initiate the stress response.

To identify proteins involved in the communication of mitochondrial stress, Fessler et al. designed a genetic screen using haploid human HAP1 cells with a cell stress response reporter. They generated mutants using a gene trap approach, then subjected each clone to one of three chemical stresses (tunicamycin, CDDO, and CCCP) and assayed the effect on initiating the integrated stress response via their reporter. Using three separate treatments allowed them to filter out global regulators and identify mechanism-specific stress regulators. To find regulators of ionophore-induced mitochondrial stress, they focused on the signature of CCCP, a drug that disrupts oxidative phosphorylation and causes immense mitochondrial stress. Two proteins were enriched in their analysis: DELE1 and HRI. After confirming their roles in mediating the stress response using different cell lines and other methods of inducing mitochondrial stress, they investigated the relationship between DELE1 and HRI. Using a series of genetic experiments with DELE1 and HRI knockouts, they found that HRI expression can rescue induction of the stress response, but DELE1 expression cannot rescue HRI knockouts. Additionally, removing the DELE1 mitochondrial targeting sequence constitutively activated the stress response. These results raised the possibility that translocation of DELE1 conveys the message of mitochondrial stress to HRI. Consistent with this, DELE1 is cleaved and observed in the cytosol upon CCCP treatment. Additionally, immunoprecipitation and mutagenesis experiments revealed that cleaved DELE1 directly binds to HRI under stress. To link DELE1 to the initial mitochondrial stress, they investigated whether mitochondrial stress-induced protease OMA1 has an impact on this protein. They found that knocking out OMA1 abrogated cleavage of DELE1 under various types of mitochondrial stress. Fessler et al.’s experiments suggest a model where mitochondrial stress leads to OMA1 activation and cleavage of DELE1, which then translocates to the cytosol to activate HRI and induce the integrated stress response.

Proteintech’s HRI/eIF2AK1 (20499-1-AP) and OMA1 (17116-1-AP) antibodies were used in this study. Anti-HRI/eIF2AK1 was used in the co-IP experiment as the pull-down antibody to show that HRI and DELE1 are binding partners. Anti-OMA1 was used in WB to monitor activation upon mitochondrial stress.

Immunohistochemical analysis of paraffin-embedded human liver tissue slide using OMA1 antibody (17116-1-AP) at dilution of 1:200.

About the corresponding author:

Lucas T. Jae, Ph.D., is a professor at the Gene Center and Department of Biochemistry at Ludwig-Maximilians-Universität München in Germany. His work focuses on uncovering the genetics of disease and mitochondrial fidelity.  


Wei  et al.

Nature Communications

Pyridoxine induces glutathione synthesis via PKM2-mediated Nrf2 transactivation and confers neuroprotection

Parkinson’s disease (PD) is a debilitating neurodegenerative disorder with limited therapeutic options. A promising area of research is the role of damage from reactive oxidative species (ROS) in the pathogenesis of this disease.Oxidative damage caused by ROS in patients’ brains are thought to be one of the main underlying causes of PD. A major player in maintaining healthy levels of ROS is glutathione, a reducing agent.

To study the role of glutathione in PD pathogenesis, Wei and colleagues (PMID: 32071304) recently examined molecular causes of glutathione deficiency occurring in patients with PD. Using agonists and antagonists of dopamine receptors, they identified that activation of dopamine D2 receptor (DRD2) in astrocytes activates glutathione synthesis both in vitro and in vivo. RNA sequencing of astrocytes revealed that glutathione production in response to DRD2 stimulation is mediated by a transcription factor Nrf2. Pull-down studies using anti-Nrf2 antibody combined with mass spectrometry identify an important cofactor, PKM2, whose dimerization is mediated by β-arrestin-mediated D2D2 signaling. Dependence of glutathione levels in astrocytes on dopamine explains its lower levels in patients with PD. Supplementation with pyridoxine, which promotes DMD2 dimerization, resulted in higher glutathione levels in cultured astrocytes, as well as reduced dopaminergic neuron loss in the mouse model of PD.

Proteintech’s rabbit anti-NRF2 (16396-1-AP) was used in this study to identify its binding partners co-regulating glutathione synthesis. In chromatin immunoprecipitation assays they identified DNA sites associated with activated Nrf2 and in a proximity ligation assay to demonstrate interaction between Nrf2 and PKM2 in astrocytes nuclei.

Proteintech’s rabbit anti-GCLC (12601-1-AP) was used to examine effects on glutathione synthesis. GCLC is a rate-limiting enzyme in glutathione biosynthesis.

Proteintech’s rabbit anti-GCLM (14241-1-AP) was used to examine effects on glutathione synthesis. GCLM is a rate-limiting enzyme in glutathione biosynthesis.

About the corresponding author: 

Gang Hu works at the Department of Pharmacology at universities in Nanjing and focuses on studying astrocyte biology, signaling, microRNA-mediated regulation of gene expression and Parkinson’s disease.


Wang et al.

Cell Stem Cell

Increased Neural Progenitor Proliferation in a hiPSC Model of Autism Induces Replication Stress-Associated Genome Instability

Autism spectrum disorder (ASD) is a neurodevelopmental disorder affecting millions globally. How the growth and function of neurons are impacted during embryogenesis is a key question in the field.

Previously, studies have found a correlation between macroencephaly and autism, suggesting a link between increased proliferation and loss of neuronal function. In the cover story for Cell Stem Cell, Wang et al. suggest that an accumulation of double-strand breaks owing to rapid S phase progression impairs the functional and structural characteristics of developing neurons in ASD.

To study the relationship between proliferation and genomic instability in ASD, Wang et al. first compared the replication stress of ASD-derived neural progenitor cells (NPCs) to control patient-derived NPCs. Using a pulse-chase experiment with different thymidine analogs, they discovered that ASD-derived NPCs have more replication forks and origins of replication, which are characteristic of replication stress. Additionally, ASD-derived NPCs have higher levels of global DNA damage markers. To determine the genomic regions most impacted by this replication stress, they performed an assay to identify double-strand breaks upon pharmacologically induced replication stress in NPCs. Wang et al. found that replication stress causes double-strand breaks in a specific subset of neural genes. Since these genes are highly expressed, they then tested for the possibility that the transcription and replication machineries were interfering with one another and causing double-strand breaks. Using a proximity ligation assay, they found high congestion of transcription and replication machinery under replication stress conditions. Analyzing the ontology of these genes, Wang et al. found that they are key structural components for cell-cell adhesion, migration, and dendrite formation. To test the link between these breaks and neurodevelopment, they assayed the ability of NPCs to form rosettes and migrate under replication stress. Rosette formation was disrupted under replication stress and migration from the neurosphere was significantly less. Overall, their work suggests that replication stress induces double-strand breaks in highly expressed genes and that relieving replication stress may be a therapeutic approach early on in ASD.          

Proteintech’s HumanKine Noggin (HZ-1118) was used in this study to differentiate Hues6 cells into embryoid bodies for the rosette assay. 

About the corresponding author: 

Fred Gage, PhD, is the President of the Salk Institute for Biological Studies and the Adler Chair Professor for Research on Age-related Neurodegenerative Disease. His research focus is understanding neurodevelopment.


Momcilovic et al


In vivo imaging of mitochondrial membrane potential in non-small-cell lung cancer

Reprogramming of cellular energetics is one of the hallmarks of cancer (PMID 21376230). Visualizing these changes in vivo in patients would advance personalized medicine for diagnosing and treating cancer. In a recent Nature paper, Momcilovic et al. demonstrated that a fluoride radiotracer (18F-BnTP) can be used to monitor the abnormal mitochondrial activity of cancer cells with positron emission tomography (PET) scanning.

To assess its applicability for lung cancers, the authors first examined the biodistribution of 18F-BnTP in a KRAS mouse model. They found that the tracer localizes to lung tumors with a preference for adenocarcinoma (ADC) over squamous cell carcinoma (SCC), suggesting its application as a non-invasive diagnostic. Using pharmacological methods to suppress or enhance oxidative phosphorylation, they showed that tracer uptake is proportional to mitochondrial activity. Combining another tracer for glucose metabolism, 18F-FDG, with 18F-BnTP predicted the efficacy of different drug combinations. Overall, this work suggests that 18F-BnTP may be useful for diagnosing and guiding the treatment of cancer.

Proteintech’s NDUFV1 (11238-1-AP), TIM23 (11123-1-AP), TOM70 (14528-1-AP), and TOM40 (18409-1-AP) antibodies were used in this study in WB to show that the 18F-BnTP signal is a reflection of mitochondrial function and can be used to differentiate ADC’s and SCC’s.  

Proteintech's TOM70 Antibody

Catalog number: 14528-1-AP

KD/KO Validated

23 Publications

Immunofluorescent analysis of ( 4% PFA ) fixed HepG2 cells using 14528-1-AP(TOM70 antibody) at dilution of 1:100 and Alexa Fluor 488-conjugated AffiniPure Goat Anti-Rabbit IgG(H+L)

IF staining of HepG2 cells using 14528-1-AP

About the corresponding author: 

David Shackleford, Ph.D., is an associate adjunct professor in the division of Pulmonary and Critical Care Medicine in the Department of Medicine at the David Geffen School of Medicine at the University of California, Los Angeles. His research focuses on cancer metabolism.


Morris et al 


α-Ketoglutarate links p53 to cell fate during tumor suppression

P53 is a famous tumor suppressor and is the most frequently mutated gene across a range of cancers. Although best known for its protective role in the DNA damage response, P53 has also recently been shown to affect cell metabolism. In a recent Nature paper (PMID: 31534224), Morris et al. showed that in pancreatic ductal adenocarcinoma (PDAC), P53 promotes a metabolic profile that inhibits tumor progression.

To determine the role of P53 in cancer metabolism, they modified a PDAC mouse model with a doxycycline-regulated shRNA targeting P53. With doxycycline treatment knocking down P53, tumors progressed rapidly to the malignant state; however, the subsequent restoration of P53 expression in the samples led to decreased tumor size and mortality. Comparing the tumor cells before and after doxycycline removal revealed a change in the metabolic profile characterized by an increase in the alpha-ketoglutarate (aKG) to succinate ratio, a key parameter controlling tumor fate.

In order to demonstrate that increased aKG was the major metabolic mediator of P53 in their model, they added aKG to PDAC cells directly and found it to have the same effects on gene expression and metabolism as restoring P53 expression. This was also observed when increasing aKG levels through the manipulation of Krebs cycle enzymes. Linking this metabolic shift to transcriptional reprogramming, Morris et al. then showed that aKG and P53 levels control the activity of aKG-dependent 5hmc epigenetic writers and that 5hmc levels are negatively correlated with the progression of disease. Thus, this work creates possibilities for novel metabolic approaches for treating PDAC and potentially other cancers that depend on P53 loss for progression.

Two Proteintech antibodies were used in this study: IDH1 (12332-1-AP) and OGDH (15212-1-AP). Both antibodies were utilized to confirm the efficiency of the doxycycline-regulated shRNA models used in their major experiments. 12332-1-AP has been validated in WB and ELISA, while 15212-1-AP has been validated in WB, ELISA, and IHC. The specificity of both antibodies has been demonstrated by KD/KO validation.

Proteintech's OGDH Antibody

Catalog number: 15212-1-AP

KD/KO Validated

18 Publications

Immunofluorescent analysis of 4% PFA fixed HeLa cells stained for anti-OGDH (15212-1-AP, 1:50, green) and anti-alpha tubulin (66031-1-IG, 1:100, red). DNA is stained by DAPI (blue).

IF staining of HeLa cells using 15212-1-AP

About the corresponding author: 

Scott Lowe, PhD, is a professor at Memorial Sloan Kettering, chair of the Geoffrey Beene Cancer Research Center, and a Howard Hughes Medical Institute investigator. His work focuses on how the genetics of cancer cells enable tumorigenesis.

Fibroblast Growth Factor 21 Drives Dynamics of Local and Systemic Stress Responses in Mitochondrial Myopathy with mtDNA Deletions.

Cell Metabolism

Forsström et al.

In a recent paper (PMID: 31523008) Forsström and colleagues examined the molecular causes of mitochondrial myopathies (MM), a class of neuromuscular diseases. The genetic cause of MM is mitochondrial DNA (mtDNA) defects. To better understand the etiology, Forsström et al. focused on the mitochondrial integrated stress response (ISRmt), a major metabolic cellular response to mtDNA mutations and alterations of mtDNA expression. In this study, they analyzed the effects of alterations of transcription factors, regulatory enzymes, and mechanistic target of rapamycin (mTOR) signaling in an in vivo mouse model and in biopsies of MM patients. They discovered that the early stages of the disease were characterized by increased levels of fibroblast growth factor 21 (FGF21) expression, which regulates ISRmt. Knocking out FGF21 resulted in a milder disease phenotype compared to controls in a MM mouse model. Elevated levels of FGF21 was shown to increase glucose uptake, serine de novo biosynthesis, and transsulfuration, which are characteristics of metabolic changes seen in MM, but it had no effect on the accumulation of mtDNA defects. The role of FGF21 depends on cell-type with the greatest impact on muscle cells and the dorsal hippocampus but little in fibroblasts. These findings raise the possibility of targeting FGF21 expression levels and function in individuals affected by MM.

Proteintech’s rabbit anti-MTHFD1L (16113-1-AP) was used in this study to examine the effects of FGF21 on the mitochondrial folate cycle. The authors determined that the expression of MTHFD1L (monofunctional C1-tetrahydrofolate synthase, mitochondrial), an enzyme converting glycine into formate, is regulated by FGF21. MTHFD1L antibody has been validated in Western blot, immunohistochemistry, ELISA, and immunoprecipitation, being specific for human, mouse, and rat.

Proteintech’s rabbit anti-CSE (12217-1-AP; Figure 1) was used in this study to examine transsulfuration in MM. The authors have shown that gamma cystathionase (CSE), an enzyme in the transsulfuration pathway, is elevated in MM patients and the MM mouse model and is regulated by FGF21. CSE antibody has been validated in Western blot, immunohistochemistry, ELISA, flow cytometry, immunofluorescence, and immunoprecipitation, being specific for human, mouse, rat, and rabbit.

Proteintech’s rabbit anti-CLPP (15698-1-AP) was used in this study as a marker of mitochondrial unfolded protein response (UPRmt). The authors have shown that caseinolytic mitochondrial matrix peptidase (CLPP), an early marker of UPRmt, is not part of ISRmt. CSE antibody has been validated in Western blot, immunohistochemistry, ELISA, immunofluorescence, and immunoprecipitation, being specific for human, mouse, rat, and zebrafish.

Proteintech's Gamma Cystathionase Antibody

Catalog number: 12217-1-AP

KD/KO Validated

88 Publications

Figure 1. Immunofluorescent analysis of (-20°C Ethanol) fixed HepG2 cells using 12217-1-AP (Gamma cystathionase antibody) at dilution of 1:50 and Alexa Fluor 488-conjugated AffiniPure Goat Anti-Rabbit IgG(H+L)


Protein kinase N controls a lysosomal lipid switch to facilitate nutrient signalling via mTORC1.

Nat Cell Biol. 2019

Wallroth et al.

Mechanistic target of rapamycin (mTOR) signaling, mediated by mTORC1 and mTORC2 protein complexes, regulates a number of vital cellular processes. mTORC1 mainly acts as a nutrient sensor controlling rates of protein synthesis, cell growth, and autophagy.

In a recent Nature Cell Biology paper (PMID: 31451768), Wallroth and colleagues discovered that protein kinase N (PKN2), upon activation via mTORC2, positively regulates mTORC1 nutrient signaling by phosphorylating PI3KC2-β enzyme. PI3KC2-β is responsible for the synthesis of phosphatidylinositol- 3,4-bisphosphate at late endosomes and lysosomes, which then represses mTORC1 activity. However, PI3KC2-β, upon phosphorylation by PKN2, is sequestered in the cytoplasm by binding to 14-3-3 proteins, in turn preventing its inhibitory action on mTORC1 signaling. This signaling pathway was dissected using gain-of-function and loss-of-function cell models (engineered cell lines expressing tagged proteins, transient overexpression of protein mutants, depletion by siRNA, and studying KO cells) coupled with immunoblotting, immunoprecipitation, and immunofluorescence studies. This newly uncovered mechanism of active mTORC2’s influence on mTORC1 signaling represents a parallel route of mTORC1 activation by mitogens, which is classically attributed to AKT activation. Therefore, PKN2 may be an interesting drug target in diseases with altered nutrient signaling, e.g., in cancer or metabolic disorders – diabetes.

Proteintech’s rabbit anti-Rab35 antibody (11329-2-AP) was used in this study to examine the association of PI3KC2-β with various endosomal Rab GTPases. Rab35 is involved in the rapid recycling of receptors from early endosomes, as well as the transport of receptors from Rab11-positive recycling endosomes. Rab35 antibody has been validated in Western blot, immunohistochemistry, immunofluorescence, and immunoprecipitation, being specific for human, mouse, and rat forms of this protein.

Proteintech's RAB35 Antibody

Catalog number: 11329-2-AP

KD/KO Validated

26 Publications

Immunohistochemical analysis of paraffin-embedded human breast cancer tissue slide using 11329-2-AP (RAB35 antibody) at a dilution of 1:200 (under 40x lens) heat mediated antigen retrieved with Tris-EDTA buffer(pH9).


BCAA catabolism in brown fat controls energy homeostasis through SLC25A44

Yoneshiro et al


Warm-blooded, or endothermic, animals use a variety of mechanisms to maintain a constant core temperature. Brown adipose tissue (BAT) is the major organ involved in this process. To generate heat, BAT uncouples oxidative phosphorylation in the mitochondria from ATP generation, resulting in heat rather than stored energy. BAT is thought to exclusively use lipids and carbohydrates as fuel. However, writing in Nature, Yoneshiro et al. suggest that BAT also uses branched-chain amino acids (BCAAs) to generate heat under cold conditions and that inhibiting the use of this fuel source results in diabetes and glucose intolerance.

To gain insight into BAT function, Yoneshiro et al. first determined the metabolic differences between humans with high BAT activity. They found that individuals with high BAT activity have lower BCAA levels after cold exposure than those with low BAT activity. To test whether it is BAT that is responsible for breaking down BCAAs in cold conditions, Yoneshiro et al developed mice that lack the ability to catabolize BCAAs specifically in BAT. Consistent with this hypothesis, they found that BCAA levels do not change in these mice after cold stimulation. Additionally, disabling BCAA metabolism in BAT resulted in glucose intolerance and diet-induced obesity. Using a series of genetic and biochemical experiments, they showed that SLC25A44 is the key transporter of BCAAs into BAT mitochondria. Additionally, mice with knocked-down SLC25A44 have a lower core body temperature and cannot metabolize BCAAs after cold exposure. Overall, Yoneshiro et al.’s work uncovers a critical fuel source of BAT and may lead to insights into obesity and metabolic syndrome.

Proteintech’s anti-TOM20 antibody (11802-1-AP) was used as a mitochondrial marker to show that SLC25A44 is localized to this organelle and as a mitochondrial loading control. This antibody has been tested for WB, IP, IHC, IF, FC, and ELISA, in addition to KD/KO validation.

Proteintech's anti-TOM20

Catalog number : 11802-1-AP

KD/KO Validated

Citations: 78

Tested Applications: WB, IP, IHC, IF, FC, ELISA

Immunofluorescent analysis of ( 4% PFA ) fixed HepG2 cells using 11802-1-AP(TOM20 antibody) at dilution of 1:50 and Alexa Fluor 488-conjugated AffiniPure Goat Anti-Rabbit IgG(H+L)


The Polycomb Repressor Complex 1 Drives Double-Negative Prostate Cancer Metastasis by Coordinating Stemness and Immune Suppression.  (PMID: 31327655)

Su et al

Cancer Cell

Prostate cancer is a leading cause of death in men worldwide. Despite the development of powerful immunotherapeutics, the immunosuppressive tumor microenvironment of prostate cancer metastases blunts the therapeutic response. In Cancer Cell, Su and colleagues show that hyperactivity of the polycomb repressor complex (PRC1) increases the expression of chemokines that attract Tregs and promote self-renewal of prostate cancer metastases (PMID 31327655).

Following on from previous work implicating PRC1 in prostate cancer tumorigenesis and metastasis, Su et al. began by comparing PRC1 levels in metastatic prostate cancer to other prostate cancer types and found that PRC1 is upregulated in metastatic samples. To test whether PRC1 is necessary for metastasis, they injected PC3 cells with knocked-down PRC1 into mice and discovered that metastatic lesions were decreased. Mechanistically, they found that PRC1 upregulation in cancer increases CCL2, which promotes stemness and recruits tumor-associated macrophages and Tregs to suppress the immune response. Demonstrating the potential clinical relevance of this result, the inhibition of PRC1 using a small molecule decreased metastasis and improved the efficacy of existing immunotherapeutics. Overall, Su et al.’s work opens the door to novel epigenetic approaches for combating metastasis, while PRC1 hyperactivity may be a common tumorigenic mechanism.

PRC1 is comprised of several subunits, among which RNF2 is critical to its activity. Proteintech’s anti-RNF2 antibody (16031-1-AP) was used to confirm the effectiveness of the investigators’ shRNA constructs targeting this protein and thereby disabling the complex. This antibody has been validated in WB, IP, IHC, IF, and ELISA.

Proteintech's   RNF2 Antibody

Catalog number :   16031-1-AP

KD/KO Validated

Citations: 3

Tested Applications: WB, IP, IHC, IF, ELISA

human brain tissue were subjected to SDS PAGE followed by western blot with 16031-1-AP(RNF2 antibody) at dilution of 1:300 incubated at room temperature for 1.5 hours


Meningeal lymphatic vessels at the skull base drain cerebrospinal fluid (PMID: 31341278)

Ahn et al.

Nature. 2019

The clearance of macromolecules from cerebrospinal fluid (CSF) is crucial for the health of the brain. Impaired clearance may play a role in the pathogenesis of Alzheimer’s disease and other neurodegenerative diseases.

The current issue of Nature (PMID: 31341278) highlights the work of Ahn et al. on meningeal lymphatic vessels (mLVs) and their differential involvement in CSF drainage into cervical lymph nodes (cLN). Experimental investigation into mLVs up to this point has been based on dorsal mLVs, which are easily accessible but whose involvement in CSF drainage could not be proven. Gaining access to basal mLVs was more demanding due to their location at the skull base, close to an accumulation of blood vessels and cranial nerves. In this study, Ahn et al. found a method of overcoming these historical experimental limitations to the investigation of basal mLVs and compared the morphology and function of dorsal versus basal mLVs. Histological examinations of dorsal and basal mLVs revealed major differences. Basal mLVs exhibited an abundant number of branches that are similar to functional LVs and far better suited to the uptake of CSF than dorsal mLVs. Basal mLVs display properties of lymphatic pre-collectors due to their lack of SMCs, the mix of button and zipper-like endothelial cell junctions, and the occurrence of valves. In another approach, the authors tracked the lymphatic outflow of the CSF as well as the clearance of macromolecules from the CSF. Starting from the cisterna magna, the signal intensities of both, CSF contrast and macromolecular tracer, peaked in basal mLVs shortly after injection. In dorsal mLVs, the lymphatic outflow peaked relatively late, while uptake of the macromolecular tracer could not be detected, thus emphasizing the importance of basal over dorsal mLVs in CSF clearance.

Many neurodegenerative diseases are related to aging, where reduction of CSF clearance could be connected to mLV remodeling. Deletion of vascular endothelial growth factor 3 (VEGF3, a key player in mLV remodeling) in mice leads to regression of dorsal mLVs before basal mLVs are affected. No impairment of CSF clearance could be detected after regression of dorsal mLVs only; on the contrary, CSF clearance was reduced once VEGF3 deletion started to affect basal mLVs. These observations are an important starting point in tackling the connection between CSF clearance from brain-damaging macromolecules and many age-related pathologies.

Proteintech’s anti-PROX1 antibody (Cat# 11067-2-AP) was used as an immunofluorescence marker for the lymphatic endothelium in morphological studies comparing dorsal and basal mLVs. This antibody has been validated in Western Blot, immunofluorescence, flow cytometry, ChIP, and ELISA.

Proteintech's anti-PROX1 antibody

Catalog number :   11067-2-AP

KD/KO Validated

Citations: 15

Tested Applications: WB, IF, FC, CHIP, ELISA

Western blot image:

HepG2 cells were subjected to SDS PAGE followed by western blot with 11067-2-AP (PROX1 Antibody) at dilution of 1:600 incubated at room temperature for 1.5 hours.


m6A enhances the phase separation potential of mRNA (PMID: 31292544)

Nature. 2019

Adapting for change is the key job of cells. In the last decade, researchers have discovered a new tool to dynamically influence the transcriptome to fine-tune cellular responses: methylated adenine or N6-methyladenosine (m6a). Advances in sequencing technologies have revealed that this epigenetic mark is abundant throughout the transcriptome and has been implicated in diverse processes including differentiation or the stress-response. The main question in the field is how this small chemical modification can have such powerful effects on the cell.

In a recent Nature paper (PMID: 31292544), Ries et al. show that m6a-RNA can be sequestered by their epigenetic readers into different phase-separated compartments during cell stress.

In an elegant set of biochemical experiments, the authors first showed that the m6a-RNA readers, YTHDF1-3, can reversibly separate into a different liquid phase from HEPES buffer by adjusting heat or salt. Afterwards, they found that heat shocks cause this protein to localize to stress granules in a separate liquid phase compartment with the aid of m6a-RNA. Using a METTL14 KO mutant that cannot catalyze m6a markings, they discovered that interaction between m6a and YTHDF1-3 is required for m6a-mRNA transcripts to be concentrated in stress granules during heat and chemical shocks. Ries et al.’s work suggests that m6a may be used to mark transcripts for protection during cellular stress and might be a mechanism for disease pathogenesis and tissue differentiation. 

Proteintech’s YTHDF1 (17479-1-AP), YTHDF2 (24744-1-AP), and G3BP1 (13057-2-AP) antibodies were used in this study. 17479-1-AP and 24744-1-AP were used throughout the study to visualize YTHDF1-2 in mouse embryonic stem cells, U2OS, NIH3T3, and HEK293 cells. 13057-1-AP was used as a marker of stress granule formation. All three of these antibodies have been validated by KD/KO experiments to demonstrate specificity.

Proteintech's   YTHDF1 Antibody

Catalog number: 17479-1-AP

KD/KO Validated

Citations: 22

Tested Applications: WB, IP, IF, IHC, ELISA

Western blot image:

WB result of YTHDF1 antibody (17479-1-AP; 1:4000; incubated at room temperature for 1.5 hours) with sh-Control and sh-YTHDF1 transfected HepG2 cells.



Hypomorphic mutations of TRIP11 cause odontochondrodysplasia. (PMID: 30728324)

Wehrle et al. 

JCI Insight. 2019

The molecular causes of many human genetic diseases are yet to be identified. In a recent paper (PMID: 30728324), Wehrle and colleagues show that odontochondrodysplasia (ODCD), a form of skeletal dysplasia, is caused by hypomorphic mutations in the TRIP11 gene. TRIP11 encodes GMAP-210 (Golgi-associated microtubule-binding protein 210) which regulates protein transport and posttranslational modification within the Golgi apparatus. Severely reduced levels of GMAP-210 in patients’ cells disrupt the structure of the Golgi apparatus and abnormal glycosylation of cargo proteins, which negatively impacts chondrocyte differentiation.

The authors investigated posttranslational modifications of protein using western blotting and analyzing band patterns of glycosylated protein species and the resulting shifts of their molecular weights. Immunofluorescence imaging was used to look at the co-localization studies of Golgi proteins and IFT20, a binding partner of GMAP-210 that localizes both to the Golgi and primary cilium.

Proteintech’s rabbit anti-IFT20 antibody (13615-1-AP) was used in this study to show that GMAP-210 protein mediates correct subcellular localization of IFT20 to the Golgi apparatus. This antibody has been validated in western blot, immunohistochemistry, and chromatin immunoprecipitation with genetic knockdown data to demonstrate its specificity.

Proteintech's  IFT20 Antibody

KD/KO Validated

Catalog number: 13615-1-AP

Citations: 31

Tested Applications: WB, IP, IHC, IF, ELISA

IF image: Immunofluorescent analysis of (10% Formaldehyde) fixed MDCK cells using 13615-1-AP (IFT20 antibody) at dilution of 1:100 and Alexa Fluor 488-conjugated AffiniPure Goat Anti-Rabbit IgG(H+L)

Reviews: 5 star

Verified customer: "Excellent for IF labelling of the Golgi under PFA fixation."

For more cilia-related antibodies, please see our cilia card.

Additionally, Proteintech’s rabbit anti-decorin antibody (14667-1-AP) was used to look at posttranslational modifications of extracellular matrix components.


This weeks Publication Spotlight features  research from  the cover of July's  issue of Cell Stem Cell  (PMID: 31080134).

Cell Stem Cell. 2019

Single-Cell Analysis of the Liver Epithelium Reveals Dynamic Heterogeneity and an Essential Role for YAP in Homeostasis and Regeneration.

The liver plays a crucial role in protein, carbohydrate, and lipid metabolism, the detoxification of drugs, and the breakdown of hormones. Two cell types, hepatocytes and biliary epithelial cells (BECs), are critical to the regenerating capabilities of the liver.

The current issue of Cell Stem Cell (Vol. 25, issue 1) features the work of Pepe-Mooney and coworkers who elucidated the dual role of the YAP signaling pathway in liver cell homeostasis and the initiation of regenerative processes (PMID: 31080134). YAP is a transcription factor that is involved in the regulation of cell proliferation as well as apoptosis. In an elegant assay, the authors utilized FACS followed by a single-cell RNA-seq to compare the expression profiles of 2,344 homeostatic BECs. Upon the differential expression of several YAP target genes, they identified two major cell clusters, YAP activated and non-activated cells. To identify the reason for this heterogeneity in YAP expression, the assay was repeated for BECs and hepatocytes after drug-induced mimicking of chronic liver damage in vivo. The results revealed the importance of YAP expression in the regenerative response of BECs and hepatocytes under liver-damaging conditions. The exposure of BECs to physiological levels of bile acid (BA) revealed the additional role of the YAP signaling pathway in cell homeostasis, dependent on intracellular BA uptake. This study presents a great basis for further investigations to elucidate cell type-dependent roles and the complexity of YAP signaling.

Beside the two major clusters, the initial RNA-seq screening revealed a small subset of cells co-expressing Dmbt1 and Ly6d, which are markers for extrahepatic BECs.

Proteintech’s Rabbit anti-LY6D (Cat# 17361-1-AP) was used for immunofluorescence staining as a differential marker for extrahepatic BECs. Based on the antibody performance it was possible to separate extrahepatic from intrahepatic BECs. This antibody has additionally been validated in Western Blot, immunohistochemistry, and ELISA.

Proteintech's LY6D Antibody

Catalog number: 17361-1-AP

Citations: 1

Tested Applications:  WB, IHC, ELISA

IHC image:

Immunohistochemical analysis of paraffin-embedded human tonsillitis tissue slide using 17361-1-AP( LY6D Antibody) at dilution of 1:50 (under 40x lens)


The first Publication Spotlight kicks off with research featured on the cover of July’s edition of 'Molecular Cell' (PMID: 31056445).

Mol Cell. 

Maintenance of CTCF- and Transcription Factor-Mediated Interactions from the Gametes to the Early Mouse Embryo

Is a child being born to a home with food insecurity? A frigid climate? A place with high toxic exposure? Being able to endow children with genetic adaptations to the environment provides significant evolutionary fitness. The prevailing notion is that these tweaks in the gamete stage are mediated by methylation and histone modifications. In the cover story for July’s Molecular Cell (PMID: 31056445), Jung et al. suggest that transcription factor sites and enhancer loops are also inherited from the parents.

Using a transposon accessibility assay and ChIP-seq, they show that mature sperm have transcription machinery and enhancer loops at many sites, but that the corresponding genes are not actively transcribed until embryogenesis. Comparing the loops of DNA in the parental gametes and embryos, they further showed that many of the CCCTC-binding factor (CTCF) and other transcription factor loops are inherited in a parent-specific manner. Their work introduces chromatin structure and early transcription factor priming as novel parental imprinting mechanisms for further investigation.

Proteintech’s Znf143 antibody (16618-1-AP) was used in this study to show that Zinc-finger transcription factors are present at many of inherited sites. This antibody has been validated in Western blot, immunohistochemistry and chromatin immunoprecipitation with genetic knockdown data to demonstrate its specificity.   

Proteintech's  Znf143 Antibody

Catalog number: 16618-1-AP

KD/KO Validated

Citations: 5

Tested Applications: WB, IHC, ChIP

Western blot image:

Mouse brain tissue were subjected SDS PAGE followed by Western blot with 16618-1-AP (Znf143 antibody) at dilution of 1:300 incubated at room temperature for 1.5 hours.

Feifan Guo. Professor Guo is a professor at the Shanghai Institute of Nutrition and Health, and her work focuses on the molecular mechanisms underlying nutrition-related metabolic diseases.

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