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These data can be used to predict variability in the metabolism of UGT2B17 substrates.
Clopidogrel carboxylic acid is metabolized mainly by UGT2B7 and UGT2B4 in the liver and by UGT2B17 in the small intestinal wall.
UGT2B17 was deleted in 64% of children with lymphoblastic malignancy, but in 83% of children with non-lymphoblastic malignancy. UGT2B17 deletion polymorphism may improve the relapse-free rate in children with non-lymphoblastic malignancy.
Study provides the first evidence of null genotype involvement in UGT2B17 as a risk factor for benign prostatic hyperplasia.
the UGT2B15 and UGT2B17 enzymes are transcriptionally regulated by sex hormone signaling in ERalpha+ breast cancer cells and are highly expressed in a subset of primary breast cancers.
Chronic lymphocytic leukemia patients with high UGT2B17 and LPL expression have significantly reduced survival.
UGT2B17 contributes to the in-vitro glucuronidation of arctigenin in liver/intestinal microsomes.
GC-C-IRMS analysis sensitive to testosterone doping independent of UGT2B17 genotype.
UGT2B17 mismatch has a negative clinical impact in allogeneic HSCT from HLA-identical sibling donors only when a male donor is used.
This descriptive study examines correlations between concentrations of tamoxifen's glucuronide metabolites and genotypes UGT1A4, UGT2B7, UGT2B15 and UGT2B17 in 132 patients with estrogen receptor-positive breast cancer under treatment with tamoxifen.
miR-376c is inversely linked to UGT2B15 and UGT2B17 expression in high-grade prostate cancer and metastasis.UGT2B15 and UGT2B17 genes are direct targets of miR-376c and thus may influence steroid metabolism during prostate cancer progression.
UGT2B17 deletion polymorphisms are associated with the risk of developing pancreatic cancer in Chinese Han population, especially in the female population.
UGT2B17-deletion interacting with p16 (+) may modify effects of smoking on TP53-mutations and may further interact with the disruptive TP53-mutations to raise relapse rates among Japanese patients with head and neck squamous cell carcinomas.
These data suggest that UGT2B17 deletion leads to reduced UGT2B17 activity, and lower BMI in male individuals. This is consistent with the hypothesis that reduced UGT2B17-mediated testosterone excretion results in higher testosterone levels
Expression of UGT2B15 and UGT2B17 is negatively regulated by the binding of miR-376c.
The UGT2B17 deletion polymorphism is not associated with tumor risks.
Structural variants unique to the malignant cell line inactivated: UGT2B17, a gene that inactivates dihydrotestosterone, a known activator of prostate cancer progression.
Variation in 3HC glucuronidation activity by CYP2A6 caused by UGT2B17 gene deletions did not significantly alter nicotine metabolite ratio in smokers.
Novel associations between UGT2B15 and UGT2B17 single nucleotide polymorphism variants and prostate cancer risk.
UGT2B17 is a possible target for androgen deprivation therapy of prostate cancer.
This gene encodes a member of the uridine diphosphoglucuronosyltransferase protein family. The encoded enzyme catalyzes the transfer of glucuronic acid from uridine diphosphoglucuronic acid to a diverse array of substrates including steroid hormones and lipid-soluble drugs. This process, known as glucuronidation, is an intermediate step in the metabolism of steroids. Copy number variation in this gene is associated with susceptibility to osteoporosis.
, C19-steroid-specific UDPGT
, UDP glycosyltransferase 2 family, member B17
, UDP-glucuronosyltransferase 2B17
, UDP-glucuronyltransferase, family 2, beta-17
, UDP glycosyltransferase 2 family, polypeptide B28
, UDP glucuronosyltransferase 2 family, polypeptide B17
, UDP-glucuronosyltransferase 2B17-like
, 17-beta-hydroxysteroid specific
, 17-beta-hydroxysteroid-specific UDPGT
, UDP glucuronosyltransferase 2 family, polypeptide B5
, UDP glycosyltransferase 2 family, member 3
, UDP-glucuronosyltransferase 2B3 precursor, microsomal
, UDP-glucuronosyltransferase 2B5
, UDPGT 2B17
, UDPGT 2B3
, liver 17 beta-hydroxysteroid UDP-glucuronosyltransferase
, testosterone, dihydrotestosterone, and beta-estradiol specific
, testosterone, dihydrotestosterone, and beta-estradiol-specific UDPGT