Validation Data Gallery
|Positive WB detected in||LNCaP cells, Transfected HEK-293 cells|
|Positive IHC detected in||human prostate cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:1000-1:8000|
|Immunohistochemistry (IHC)||IHC : 1:100-1:400|
|Sample-dependent, check data in validation data gallery|
10679-1-AP targets KLK3/PSA in WB, IHC, IF, ELISA applications and shows reactivity with human samples.
|Cited Reactivity||human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||KLK3/PSA fusion protein Ag1060|
|Full Name||kallikrein-related peptidase 3|
|Calculated molecular weight||29 kDa|
|Observed molecular weight||30-34 kDa|
|GenBank accession number||BC005307|
|Gene ID (NCBI)||354|
|Purification Method||Antigen affinity purification|
|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.|
Kallikreins are a subgroup of serine proteases having diverse physiological functions. Growing evidence suggests that many kallikreins are implicated in carcinogenesis and some have potential as novel cancer and other disease biomarkers. kallikrein-related peptidase 3, which is also called PSA (prostate-specific antigen) in the clinical setting, is useful in the diagnosis and monitoring of prostatic carcinoma. KLK3 has 5 isoforms produced by alternative splicing.
ACSS3 represses prostate cancer progression through downregulating lipid droplet-associated protein PLIN3.
Clin Transl Med
Melatonin inhibits lipid accumulation to repress prostate cancer progression by mediating the epigenetic modification of CES1.
A feedback loop between the androgen receptor and 6-phosphogluoconate dehydrogenase (6PGD) drives prostate cancer growth
Mol Cancer Ther
Stem Cell Res Ther
Expansion of mouse castration-resistant intermediate prostate stem cells in vitro
Prostate cancer cell proliferation is influenced by LDL-cholesterol availability and cholesteryl ester turnover.