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The findings provide genetic and epidemiological evidence for an association of UGT1A and CCR5 polymorphisms with hepatitis B virus infection in Chinese Yi and Yao populations.
Genetic variant minor allele frequencies were similar between cases and controls, except for UGT1A1*28.
During liver ontogeny recruitment of HNF1A (show HNF1A Proteins) leads to aggregation of the cofactors MLL1, NCOA6 (show NCOA6 Proteins), and p300 (show EP300 Proteins) at the UGT1A1 promoter, which regulates histone modifications and subsequent UGT1A1 expression.
Patients who initiated atazanavir/ritonavir-containing regimens, UGT1A1 slow metabolizer genotype rs887829 T/T was associated with increased bilirubin-related discontinuation of atazanavir in White but not in Black patients, this despite T/T genotype being more frequent in Black patients.
Patients with asthenic constitution and the stigma dysplasia of connective tissue have to be examined by the presence of mutations rs8175347 gene UGT1A1. The carrier not only homozygous but with the heterozygous variant mutations may require changes in the interpretation of symptoms, lifestyle, medication, etc.
Inter-isoform Hetero-dimerization of Human UDP-Glucuronosyltransferases (UGTs) 1A1 (show SLC45A2 Proteins), 1A9, and 2B7 and Impacts on Glucuronidation Activity
Results show that the occurrence of neonatal hyperbilirubinemia of neonates was not associated with UGT1A1*28 gene polymorphism, but closely correlated with the Gly71Arg gene polymorphism. Meanwhile, the Arg allele mutation was related to the degree of jaundice.
UGT1A1 gene promoter polymorphism and G71R mutation are possible risk factors for Turkish neonates with DC(-) ABO incompatibility and unexplained hyperbilirubinemia.
The presence of the TA7 allele UGT1A1 gene promoter, responsible for higher systemic bilirubin levels, was associated with a twofold lower risk of manifestation of Fabry Disease.
results suggested that Gly71Arg and Asn130Asp mutations in UGT1A1 and OATP2 (show SLCO1B1 Proteins) genes might be involved in the development of hyperbilirubinemia in neonates.
data confirm that Ugt1a proteins are present and active in preimplantation murine embryos and point to a potential role for these proteins in implantation and early embryonic and fetal development
Intestinal induction of the UGT1A1 gene may serve to limit toxicity and improve the efficacy associated with CPT (show DHDDS Proteins)-11 colorectal cancer treatment.
Data observed that OSM (show OSM Proteins) positively augmented the CAR and UGT1A1 expressions and CAR-mediated signaling in vivo and in vitro, through cross talk between the nuclear CAR receptor and the plasma membrane OSM (show OSM Proteins) receptor, via the MAPK (show MAPK1 Proteins) cascade.
suppression of AhR (show AHR Proteins) signaling pathway is associated with the down-regulation of Ugt1a mRNA during urinary bladder carcinogenesis.
Nrf2 (show NFE2L2 Proteins)-Keap1 (show KEAP1 Proteins)-dependent UGT1A1 induction by prooxidants might represent a key adaptive response to cellular oxidative stress
the loss of UGT1A function in Ugt1(-/-) mice leads to a metabolic syndrome that can serve as a model to further investigate the toxicities associated with unconjugated bilirubin and the impact of this disease in humans.
This gene encodes a UDP-glucuronosyltransferase, an enzyme of the glucuronidation pathway that transforms small lipophilic molecules, such as steroids, bilirubin, hormones, and drugs, into water-soluble, excretable metabolites. This gene is part of a complex locus that encodes several UDP-glucuronosyltransferases. The locus includes thirteen unique alternate first exons followed by four common exons. Four of the alternate first exons are considered pseudogenes. Each of the remaining nine 5' exons may be spliced to the four common exons, resulting in nine proteins with different N-termini and identical C-termini. Each first exon encodes the substrate binding site, and is regulated by its own promoter. The preferred substrate of this enzyme is bilirubin, although it also has moderate activity with simple phenols, flavones, and C18 steroids. Mutations in this gene result in Crigler-Najjar syndromes types I and II and in Gilbert syndrome.
UDP glycosyltransferase 1 family, polypeptide A1
, UDP-glucuronosyltransferase 1-1
, UDP-glucuronosyltransferase 1-A
, UDP-glucuronosyltransferase 1A1
, bilirubin UDP-glucuronosyltransferase 1-1
, bilirubin UDP-glucuronosyltransferase isozyme 1
, bilirubin-specific UDPGT isozyme 1
, UDP-glucuronosyltransferase 1 family, member 1
, UDP-glucuronosyltransferase 1 family, polypeptide A1
, UDP glucuronosyltransferase 1 family, polypeptide A1
, uridine diphosphate glucuronosyltransferase 1A1
, UDP-glucuronosyltransferase UGT1A01
, UDP glucuronosyltransferase 1 family polypeptide A1
, UDP glycosyl transferase 1A1
, UDP-glucuronosyltransferase 1-1-like
, UDP-glucuronosyltransferase 1 family member 1