Human Polyclonal UGT1A4 Ab
- Known as:
- Human Polyclonal UGT1A4 Antibody
- Catalog number:
- a5549
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal UGT1A4
Related genes to: Human Polyclonal UGT1A4 Ab
- Gene:
- UGT1A4 NIH gene
- Name:
- UDP glucuronosyltransferase family 1 member A4
- Previous symbol:
- -
- Synonyms:
- HUG-BR2, UGT1D
- Chromosome:
- 2q37.1
- Locus Type:
- complex locus constituent
- Date approved:
- 2000-06-22
- Date modifiied:
- 2016-03-01
Related products to: Human Polyclonal UGT1A4 Ab
Related articles to: Human Polyclonal UGT1A4 Ab
- : With the ongoing efforts in supporting the discovery of novel targeted drug delivery systems for the upper region of the female reproductive tract (FRT), it is imperative to understand the local drug disposition pathways. We aim to obtain a comprehensive profile of the drug transporters and drug-metabolizing enzymes in the human ectocervix, uterus, and fallopian tubes, as these factors may substantially influence mucosal penetration, tissue exposure, drug disposition, and the risk of drug-drug interactions. Gene expression of 12 drug transporters and 21 drug-metabolizing enzymes was quantified using RT-qPCR. Protein expression of highly expressed transporters was assessed using immunohistochemistry (IHC). : Among the 12 transporters analyzed, the efflux transporters P-gp, BCRP, and MRP4 exhibited the highest expression across the ectocervix, endometrium, myometrium, and fallopian tubes, with P-gp consistently showing the greatest abundance in all evaluated FRT tissues. Expression of these transporters was significantly higher (6-17×) in myometrium compared with ectocervix. IHC demonstrated strong localization of P-gp, BCRP, and MRP4 to epithelial layers facing the lumen, as well as to stromal and vascular endothelial cells. For drug-metabolizing enzymes, all 21 phase I and II enzymes were detectable across the FRT, and 15 were expressed at comparatively higher levels across all tissue types. These included CYP1A1, CYP1B1, CYP2B6, CYP2C8, CYP2C19, CYP3A4, UGT1A1, UGT1A3, UGT1A4, UGT1A7, UGT1A8, UGT1A10, UGT2B4, UGT2B15, and UGT2B17. : The gene expression and localization data obtained from this work may improve our understanding of drug disposition in the FRT, which will inform selection, design, and optimization of drugs intended for targeted delivery within the FRT. - Source: PubMed
Publication date: 2026/05/21
Le AnValicherla Guru RZhang JunmeiWang LinDonnelly Mark KBies RobertRohan Lisa C - : Tamoxifen is widely used in the treatment of hormone receptor-positive breast cancer and has been shown to successfully reduce recurrence and mortality rates. Nonetheless, variability in patient response to tamoxifen treatment is observed with up to 40% of patients experiencing recurrence. Genetic polymorphisms in pharmacogenes encoding enzymes involved in tamoxifen metabolism have been linked to some of this observed interindividual variability. The pharmacogenetics of tamoxifen in populations of African descent remain understudied, creating difficulties in pinpointing the primary factors behind the observed variable response. To address this gap, this study aimed to investigate the role of genetic variation in tamoxifen treatment outcomes in a South African cohort. : Participants included 166 Mixed and African Ancestry breast cancer patients who had received tamoxifen treatment. Genetic characterization was performed for 53 single nucleotide polymorphisms (SNPs) and two copy number variations across eight drug-metabolizing enzymes, including cytochrome P450s (, , , ), UDP-glucuronosyltransferases (), and sulfotransferases (, , ). The association between genotypes and disease-free survival (DFS) was evaluated using Cox proportional hazards regression models. : The or * genotype showed a nominal association with improved DFS ( = 0.049), with a similar trend observed for rs11888492. In contrast, rs3775779 heterozygosity showed a nominal association with reduced DFS ( = 0.044). SNPs (rs4149393, rs4149394, rs1042157) demonstrated trends toward reduced DFS. : These exploratory findings highlight the need for more inclusive pharmacogenomic research and point to potential biomarkers for optimizing tamoxifen therapy in African populations. - Source: PubMed
Publication date: 2026/03/31
Kruger BiancaChimusa Emile RAbera Aron BSingh JesmikaShamley DelvaDandara Collet - Glucuronidation, catalysed by UGT enzymes, plays a key role in the metabolism of clozapine (CLZ) and its active metabolite, norclozapine (NCLZ). Genetic polymorphisms in UGT1A4 and UGT2B10 can influence NCLZ plasma levels. Co-administration of valproic acid (VPA), commonly used in Treatment Resistant Schizophrenia, has been linked to decreased NCLZ concentrations and increased neutropenia risk. Additionally, CYP1A2, the main enzyme responsible for CLZ N-demethylation, may affect CLZ and indirectly NCLZ levels, specially considering genetic variability and smoking status. A total of 296 plasma samples from 61 CLZ-treated patients were retrospectively analysed. CLZ and NCLZ levels were quantified using Liquid Chromatography-Tandem masses (LC-MS/MS). VPA levels were measured by Ultraviolet–Visible spectrophotometric immunoassay. Genotyping for CYP1A2*1F (rs762551) and UGT2B10*2 (rs61750900) polymorphisms was performed using Real-Time PCR and UGT1A4*3 (rs2011425) polymorphism was conducted through direct sequencing. VPA co-administration significantly reduced NCLZ levels (–49.20%, p < 0.001) with minimal impact on CLZ. CYP1A2*1F/*1F and UGT1A4*1/*3 or *3/3 were associated with lower NCLZ levels and dose-adjusted ratios (C/D). These associations were not significant in the VPA group. Absolute neutrophil count (ANC) was 15.96% lower in VPA co-treated patients (p < 0.001) and positively correlated with NCLZ levels. These results emphasize the importance of integrating pharmacogenetic and pharmacokinetic data when prescribing VPA and CLZ concomitantly, to optimize therapeutic efficacy and minimize adverse effects. - Source: PubMed
Publication date: 2026/04/24
Sangüesa EstelaCirujeda ChristineBernal AnaRibate María PilarGarcía Cristina Belén - While pregnancy-related changes in phase I enzyme activity are well-documented, less is known about the impact on phase II enzymes. This study aimed to test the hypothesis that changes in the pharmacokinetics (PK) of uridine 5'-diphosphoglucuronosyltransferase (UGT) substrates during pregnancy result from altered enzyme expression or activity. Physiologically based PK (PBPK) modelling was used to evaluate these changes in pregnant populations. - Source: PubMed
Publication date: 2026/04/15
Saffaf Williamvan der Velde YmkeMalik Paul R VPrins Jelmer RGordijn Sanne JTouw Daan JMian Paola - Uridine diphosphate (UDP)-glucuronosyltransferases (UGTs) are a family of enzymes with highly similar amino acid sequences, making it challenging to distinguish between their roles. Developing selective probes and inhibitors is essential for understanding the unique functions of each isoform. In this study, we synthesized four novel naphthalimide-based fluorescent probes bearing nitrogen-containing substituents at the 4-position and identified -butyl-4-methylpiperazine-1,8-naphthalimide (BAD3) as a highly selective and sensitive substrate for UGT1A4. Using BAD3, we established an inhibitor screening platform and identified ursolic acid (T7) as a promising lead compound from a natural product library. Structure-activity relationship (SAR) studies revealed that esterification at the 3-hydroxyl group significantly enhanced inhibitory activity, yielding two potent inhibitors, T25 and T26, while modifications at the 28-carboxyl group reduced activity. Further characterization confirmed T25 (inhibition constant ( ) = 0.64 μM) and T26 ( = 0.61 μM) as selective and competitive UGT1A4 inhibitors. Molecular docking revealed that the 28-carboxyl group plays a crucial role by forming a salt bridge with Arg258 in the UGT1A4 active site. studies demonstrated that T25 significantly altered the pharmacokinetic profile of BAD3, confirming its inhibitory effect on UGT1A4 in animals. Together, BAD3 and the selective inhibitors T25/T26 serve as valuable molecular tools for studying the physiological and pharmacological roles of UGT1A4. - Source: PubMed
Publication date: 2025/07/26
Mao NingLi Shi-QingZhou Xiang-LuHu CongWu Wen-ChaoWei HuaZou Li-WeiYang Ling