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glycosylation changes the enzymatic activity of KLK2 in a drastically substrate-dependent manner.
The results indicated that W-hK2 had a defect in cellular trafficking due to its misfolding and that it activated the unfolded protein response, suggesting a mechanism to explain the association of the T allele with higher prostate cancer risk.
miR-378 was predicted to target both KLK2 and KLK4 and downregulated levels detected in prostate cancer patients.
The differential regulation of alternative transcripts (using KLK2, KLK3 and KLK4 as models) by androgens and anti-androgens as an indicator of prostate cancers, was investigated.
Structure-function analyses of KLK2 establish the 99-loop as master regulator of its activity.
Predictions based on levels of four kallikrein markers, including KLK2, in blood distinguish between pathologically insignificant and aggressive disease after radical prostatectomy with good accuracy.
Alteration of cellular junctions in benign prostatic hyperplasia could contribute to the presence of luminal epithelial secreted proteins prostate specific antigen (PSA)2 and and KLK2 in the stromal compartment.
we present the first evidence that KLK2 can also function as an androgen receptor modulator that may modulate cell growth after the development of castration-resistant prostate cancer
Associations observed in young, healthy men between the seminal plasma and serum concentrations of hK2 and PSA and several genetic variants in KLK2 and KLK3 could be useful to refine models of PSA cutoff values in prostate cancer testing.
Genetic variants at ATF7IP and KLK2 contribute to the variance of %fPSA.
Two SNPs, in beta-microseminoprotein at and in kallikrein-related peptidase 2 at, are associated with PCA3 score at genome-wide significance level
TK promotes vessel growth by increasing the number of EPCs and enhancing their functional properties through the kinin B(2) receptor-Akt signaling pathway.
An exploratory study of a KLK2 polymorphism as a prognostic marker in prostate cancer was found to be less likely associated with low Gleason score morphology.
we identifiedand genotyped novel single-nucleotide polymorphisms in cancer cases and controls which verified prior associations in KLK2 and in MSMB (but not in KLK3) with prostate cancer
Data show six non-synonymous amino acid or frame shift changes in the KLK3 gene and three changes in each of the neighboring genes, KLK15 and KLK2.
The identification of unusual mRNA splice variants of the KLK2 and KLK3 genes that result from inclusion of intronic sequences adjacent to the first exon.
Characterization of androgen receptor and nuclear receptor co-regulator expression in human breast cancer cell lines exhibiting differential regulation of kallikreins 2 and 3.
kallikrein expression in nipple aspirate fluid- ethnic variation
Measurements of free prostate specific antigen and hK2 improve on our ability to counsel patients prior to treatment as to their risk of biochemical recurrence
An additional serum marker for the detection of prostatic cancer.
This gene encodes a member of the grandular kallikrein protein family. Kallikreins are a subgroup of serine proteases that are clustered on chromosome 19. Members of this family are involved in a diverse array of biological functions. The protein encoded by this gene is a highly active trypsin-like serine protease that selectively cleaves at arginine residues. This protein is primarily expressed in prostatic tissue and is responsible for cleaving pro-prostate-specific antigen into its enzymatically active form. This gene is highly expressed in prostate tumor cells and may be a prognostic maker for prostate cancer risk. Alternate splicing results in both coding and non-coding transcript variants.
glandular kallikrein 2
, glandular kallikrein-1
, kallikrein 2, prostatic
, tissue kallikrein-2
, arginine esterase
, S2 kallikrein
, esterase 1
, glandular kallikrein-2
, LOW QUALITY PROTEIN: kallikrein-2
, kallikrein-related peptidase 2