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UGT1A1 polymorphisms have the potential to be a prognostic marker of irinotecan treatment.
Although we have found quite a large number of genetic variants of the UGT1A1 and SLCO1B1 (show SLCO1B1 Proteins) genes in the African-American population, it does not appear that they have a significant impact on the incidence of hyperbilirubinemia among this group of infants.
it is unclear whether UGT1A1 plays a role in the development of anti-tuberculosis drug-induced hepatotoxicity in the Chinese population
The MTD (show MT1E Proteins) of irinotecan in FOLFIRI plus bevacizumab is 310 mg/m(2) for UGT1A1 *1/*1 patients and 260 mg/m(2) for *1/*28 patients. Bevacizumab does not alter the pharmacokinetics of irinotecan. The antitumor efficacy of these genotype-guided doses should be tested in future studies of patients with mCRC treated with FOLFIRI plus bevacizumab
Longer progression-free was seen in breast cancer patients who were heterozygous for a UGT1A1 mutation compared with homozygous wild-type patients when treated with irinotecan combined with S-1.
UGT1A1*6 and/or UGT1A1*28 alleles are associated with plasma dolutegravir concentrations in Japanese individuals infected with HIV-1.
The linked polymorphisms, A(TA)7TAA and c.-3279T>G, in UGT1A1, were most strongly associated with Gilbert syndrome, whereas mutations in the coding region, particularly p.G71R and p.Y486D, occurred more frequently in CNS-II. In addition, iron deposition may be more common in liver biopsies from patients with Crigler-Najjar syndrome type II.
UGT1A1*6 is a risk factor for prolonged unconjugated hyperbilirubinemia in preterm infants in Japan
Our findings indicate that regorafenib plus FOLFIRI with irinotecan dose escalation based on UGT1A1 genotyping in previously treated patients with mCRC and with UGT1A1*1/*1 and UGT1A1*1/*28 genotypes is clinically effective and yields improved oncological outcomes.
Besides G6PD (show G6PD Proteins)-deficiency screening, UGT1A1 genetic analysis, and especially the UGT1A1*6(c.211G>A, p.Arg71Gly) polymorphism detection, may be taken into consideration for early diagnosis and treatment of severe hyperbilirubinemic newborns in southern China.
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