Product Information
22667-1-AP targets FUNDC1 in WB, ELISA applications and shows reactivity with human samples.
| Tested Reactivity | human |
| Cited Reactivity | human, mouse |
| Host / Isotype | Rabbit / IgG |
| Class | Polyclonal |
| Type | Antibody |
| Immunogen |
CatNo: Ag18303 Product name: Recombinant human FUNDC1 protein Source: e coli.-derived, PGEX-4T Tag: GST Domain: 1-155 aa of BC042813 Sequence: MATRNPPPQDYESDDDSYEVLDLTEYARRHQWWNRVFGHSSGPMVEKYSVATQIVMGGVTGWCAGFLFQKVGKLAATAVGGGFLLLQIASHSGYVQIDWKRVEKDVNKAKRQIKKRANKAAPEINNLIEEATEFIKQNIVISSGFVGGFLLGLAS Predict reactive species |
| Full Name | FUN14 domain containing 1 |
| Calculated Molecular Weight | 155 aa, 17 kDa |
| GenBank Accession Number | BC042813 |
| Gene Symbol | FUNDC1 |
| Gene ID (NCBI) | 139341 |
| Conjugate | Unconjugated |
| Form | Liquid |
| Purification Method | Antigen affinity purification |
| UNIPROT ID | Q8IVP5 |
| Storage Buffer | PBS with 0.02% sodium azide and 50% glycerol, pH 7.3. |
| Storage Conditions | Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA. |
Publications
What published studies show
The FUNDC1 polyclonal antibody (Cat# 22667-1-AP) has 3 total citations. These appear in Journal of Translational Medicine, Antioxidants (Basel), and ACS Chemical Neuroscience. The associated research fields include bladder cancer progression and mitophagy, DNA damage repair and skin anti-aging via the FUNDC1-mediated mitophagy pathway, and neuroprotection against oxidative stress through autophagy and mTOR/Akt/CREB signaling.
| Species | Application | Title |
|---|---|---|
J Transl Med SRSF1-mediated alternative splicing regulates bladder cancer progression and cisplatin sensitivity through HIF1A/BNIP3/mitophagy axis | ||
Antioxidants (Basel) Camellia japonica Flower Extract and the Active Constituent Hyperoside Repair DNA Damage Through FUNDC1-Mediated Mitophagy Pathway for Skin Anti-Aging | ||
ACS Chem Neurosci Rapamycin confers neuroprotection against colistin-induced oxidative stress, mitochondria dysfunction and apoptosis through the activation of autophagy and mTOR/Akt/CREB signaling pathways. |
