UGDH antibody Polyclonal Antibodies Primary antibodies
- Known as:
- UGDH (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb101134
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- UGDH antibody Polyclonal Antibodies Primary antibodies
Related genes to: UGDH antibody Polyclonal Antibodies Primary antibodies
- Gene:
- UGDH NIH gene
- Name:
- UDP-glucose 6-dehydrogenase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p14
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-01
- Date modifiied:
- 2015-08-24
Related products to: UGDH antibody Polyclonal Antibodies Primary antibodies
Related articles to: UGDH antibody Polyclonal Antibodies Primary antibodies
- Melon (.) is a widely cultivated fruit globally, valued for its high nutritional content and diverse culinary uses. However, the molecular mechanisms underlying flavor enhancement mediated by grafting remain poorly understood. - Source: PubMed
Publication date: 2026/05/01
Zhang HaoMuhammad Mohsin KaleemLiang QiganDu YinkeMaerhaba PaerhatiTian BanlvZhang HaojieZhang WenweiHuang YuanWang MinZhu JingrongFu Xiaofa - Despite the widely reported experimental anti-tumor effects, metformin's role remains exceedingly complex, with contradictory results in clinical trials. Our study, based on metabolomics analysis of lung adenocarcinoma (LUAD) samples, xenografts, and cells, unveils a novel process that metformin promotes the conversion of UDP-glucose (UDPG) to UDP-glucuronic acid (UDPGA) in glucuronic acid metabolism. Mechanistically, metformin activates UDP-glucose 6-dehydrogenase (UGDH) through AMPK-mediated phosphorylation of UGDH(S476), a previously unstudied phosphorylation site, impeding the binding of UDP-Xyl to UGDH and the subsequent allosteric inhibition. Consequently, metformin-treated cells are more reliant on UXS1, a downstream metabolic enzyme of UGDH, for detoxifying UDPGA based on the "kitchen-sink" model. Through comprehensive virtual screening of a compound library, we identified that plantainoside is a potent UXS1-targeting agent. Remarkably, when combined with metformin, plantainoside exhibits a superior synergistic lethal effect in LUAD cells, organoids, xenografts, and spontaneous models. Moreover, this combination not only directly targets tumor cells but also synergistically boosts CD8+ T cells and suppresses the differentiation of macrophages, thereby significantly enhancing immunotherapy efficacy. Collectively, our results shed light on metformin's complicated role by revealing its novel impact on glucuronic acid metabolism and dependence on UXS1; thus, targeting UXS1 combined with metformin represents a highly promising new strategy. - Source: PubMed
Publication date: 2026/05/10
Sui QihaiChen ZhencongShan GuangyaoHu ZhengyangJin XingLiang JiaqiYi YanjunYin JiachengShi HaochunJiang XifeiXi JunjieLin ZongwuZhan ChengSun FenghaoJiang Wei - Peanut (Arachis hypogaea L.) is an important oil and economic crop, and its production has long been severely threatened by soil-borne bacterial wilt (BW) disease. However, the molecular mechanism of host resistance to it has not yet been systematically elucidated. In this study, the highly resistant peanut variety Zhonghua 6 was used as the research object. Through transcriptomic analysis, a total of 1,122 differentially expressed genes (DEGs) were identified between carefully designed treatment and control groups. WGCNA analysis led to the discovery of 14 hub genes, including two cytochrome P450 genes and a UGDH gene. Through metabolomic analysis, 1,614 differentially accumulated metabolites (DAMs) were identified, and 6-methylcoumarin, erucamide, and piceatannol were confirmed to inhibit the growth of R. solanacearum. Integrative transcriptomic and metabolomic analyses uncovered a comprehensive immune regulatory network consisted of genes involved in key pathways associated with R. solanacearum infection such as MAPK signaling, plant hormone signal transduction, phenylpropanoid biosynthesis, flavonoid biosynthesis, and ABC transporter. Overall, these results provide new insights into the molecular mechanisms governing peanut resistance to R. solanacearum, which might assist in the mining of resistance-related genes, developing of new disease control measures as well as breeding of novel disease-resistant cultivars in peanut. - Source: PubMed
Publication date: 2026/05/07
Yang PingYang QianChang YingyingLi JihuaChen RupeiGelaye YohannesLiu NianHuang LiZhou XiaojingChen WeigangYu BolunDing YingbinJiang HuifangLiao BoshouLei YongLuo Huaiyong - Jamuar syndrome (Developmental and Epileptic Encephalopathy 84, OMIM# 618792) is a rare autosomal recessive congenital disorder of glycosylation (CDG), caused by variations in the gene encoding UDP-glucose dehydrogenase (UGDH). Although a number of UGDH variants have been functionally characterized, there is an incomplete catalogue of variants and their impacts on development. Here, we present functional data characterizing new missense variants from three unrelated individuals who were D379N homozygous, Y356D homozygous, and compound heterozygous A436G/R442W, respectively. UGDH activity was low to undetectable in patient-derived fibroblasts bearing either UGDH D379N or UGDH A436G/R442W, relative to WT fibroblasts, despite robust UGDH expression in both. Measurement of nucleotide sugar levels revealed a significant decrease in the UGDH product, UDP-glucuronate, and consequent reductions in hyaluronan production, Notch1 levels, and rate of O-and N-linked glycan synthesis, consistent with loss of UGDH activity. These features support the designation of UGDH D379N and UGDH A436G as causative variants in Jamuar Syndrome. We expressed and purified UGDH D379N, A436G, R442W, R443H, and Y356D variants to examine underlying molecular mechanisms. Kinetic properties and structural stability assays selectively revealed significant changes in conformational dynamics that manifested strong effects on endogenous inhibitor binding and product inhibition. The results suggest that alterations to the C-terminal domain impact activity of UGDH in cells by impairing its cofactor exchange rate and diminishing quaternary association. These effects would be maximized at developmental milestones in which hypoxia drives morphological change, since NADH accumulation would then decrease glycosaminoglycan production, with profound developmental consequences. - Source: PubMed
Publication date: 2026/04/28
Harwood HaliZimmer Brenna MUtz Asher RVenema MyrrheAllego EmilySkirboll Sydney SHarding AutumnEnders Jeffrey RGrantham-Hill SarahElmslie FrancesLy Yong-RuClarke AntoniaXu MariaTan Hui JeenStals KarenJamuar Saumya ShekharBarakat Tahsin StefanMakris Thomas MBarycki Joseph JSimpson Melanie A - Biliary atresia (BA), the most common cause of extrahepatic obstructive jaundice in infants, is a severe infant disease with a poor prognosis and unclear etiology. RNA-binding proteins (RBPs) are key regulators of alternative splicing and are implicated in various liver pathologies. However, whether RBP dysfunction and resultant aberrant splicing contribute to BA pathogenesis remains unknown. - Source: PubMed
Publication date: 2026/04/06
Cheng JiwenZhao PuCao PingHui JunPeng