Ask about this productRelated genes to: UGT1A1 Blocking Peptide
- Gene:
- UGT1A1 NIH gene
- Name:
- UDP glucuronosyltransferase family 1 member A1
- Previous symbol:
- UGT1, GNT1
- Synonyms:
- UGT1A
- Chromosome:
- 2q37.1
- Locus Type:
- complex locus constituent
- Date approved:
- 1989-02-13
- Date modifiied:
- 2019-04-23
Related products to: UGT1A1 Blocking Peptide
Related articles to: UGT1A1 Blocking Peptide
- Low phospholipid-associated cholelithiasis (LPAC) syndrome is a rare inherited disorder caused by mutations with heterogeneous manifestations. We describe two LPAC cases in a mother-son pair, detailing their clinical presentations, diagnostic evaluations, and management. A novel frameshift variant (c.715_716insTT; p.Ser239PhefsTer9) was identified, expanding the genetic spectrum of LPAC syndrome. - Source: PubMed
Publication date: 2026/10/02
Yang Hui-MingLiu JunZhang Zheng - Mycophenolic acid (MPA), a first-line immunosuppressant for preventing transplant organ rejection, exhibits substantial inter- and intra-individual pharmacokinetic variability. We hypothesized that music elements (tempo, rhythm, and harmony) can affect the formation of MPA glucuronide (the major, inactive metabolite, MPAG) and MPA acyl glucuronide (the minor, toxic metabolite, AcMPAG) in Sprague Dawley (SD) rats. - Source: PubMed
Publication date: 2026/09/17
Adhiya JinalShalaby Ali HAl-Dajani Ala'A REl-Mahrouk Sara ROlympus CarolAhonen HeidiEl-Kadi Ayman O SKiang Tony K L - Bilirubin encephalopathy (BE) is a severe neurological complication of neonatal hyperbilirubinemia, but the molecular mechanisms underlying bilirubin-induced brain injury remain unclear. We investigated whether UDP-glucuronosyltransferase 1A1 (UGT1A1) regulates neuronal ferroptosis in BE and whether this process is controlled by ten-eleven translocation methylcytosine dioxygenase 1 (TET1)-mediated demethylation. - Source: PubMed
Publication date: 2026/09/21
Yang XiaolingDuan QingmingaiLei BeibeiYan Jun - Cholestasis is characterized by impaired bile flow and intracellular bile acid accumulation, leading to progressive liver injury driven by oxidative stress, inflammation, and hepatocellular apoptosis. Disruption of canalicular bile acid transport, particularly BSEP dysfunction, represents a central initiating event in cholestatic liver damage. α-Naphthyl isothiocyanate (ANIT) is widely used to model intrahepatic cholestasis; however, the mechanisms underlying selenium-mediated protection remain incompletely defined. - Source: PubMed
Publication date: 2026/09/28
Bolat İsmailÖzdemir SelçukÇomakli SelimSağlam Yavuz SelimTekin SametÇinar BurakBolat MerveOrhan BetülSağsöz Mustafa ErdemOkkay Ufuk - St. John's Wort (SJW; ) is widely used for mild-to-moderate depression and is known to induce certain cytochrome P450 enzymes (notably CYP3A4, with reported effects on CYP2C9 and CYP2C19) and intestinal P-glycoprotein, but its effects on UDP-glucuronosyltransferases (UGTs), the principal phase-II drug-metabolizing enzymes, remain largely uncharacterized. Using recombinant human UGTs with 4-methylumbelliferone as the probe substrate, we characterized inhibition by the two major SJW constituents, hypericin and hyperforin, across eleven isoforms, and combined AlphaFold2-based molecular docking, molecular dynamics, and MM/PBSA analyses with FDA 2020 static-model extrapolation (IVIVE) to predict drug-drug interaction (DDI) risk. Both compounds were broad-spectrum UGT inhibitors, with hyperforin the most potent (UGT1A1 = 1.46 μM; UGT2B7 = 6.70 μM). On the clinically critical UGT1A1, hyperforin and hypericin occupied the aglycone pocket through two structurally distinct binding modes that both produced noncompetitive kinetics. Under a complete-dissolution assumption, IVIVE flagged hyperforin as a high-risk intestinal UGT inhibitor ( = 69.49 for UGT1A1 and 15.93 for UGT2B7, far above the FDA threshold of 11); however, incorporating hyperforin's poor (∼2%) dissolution and acid instability lowered the corrected to ∼2.0-2.9 (UGT1A1) and ∼1.2-1.4 (UGT2B7), indicating a potential rather than definitive intestinal interaction whose magnitude depends on the SJW formulation. These findings provide mechanistic and quantitative support for reported clinical SJW-drug interactions and highlight intestinal glucuronidation as a previously underappreciated SJW-mediated DDI pathway. - Source: PubMed
Publication date: 2026/09/10
Chen JinqianZhang YanlongZhao XixiCui YatingXu TongLiu LingxiaZhao ZhenyuLi Xichuan