Ask about this productRelated genes to: UGDH Blocking Peptide
- 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 Blocking Peptide
Related articles to: UGDH Blocking Peptide
- Awns are crucial spike traits in Poaceae plants and are closely associated with seed development. Griseb. is a high-quality alpine forage and an essential grass species for ecological restoration. To reveal the regulatory mechanism of awns on thousand seed weight in , 20 germplasm accessions were used as experimental materials in this study. Superior germplasms were screened via phenotypic correlation analysis. The screened superior germplasm was subjected to awned and de-awned treatments. Physiological indicators during seed development under the two treatments were measured at the milk stage, dough stage, and full ripe stage, and transcriptome sequencing was further used to identify the core regulatory pathways and key genes. The results showed that awn length was extremely significantly positively correlated with thousand seed weight ( < 0.01), and the optimal germplasm PI 655186 with superior awn length and thousand seed weight was obtained. Compared with the de-awned treatment, the awn-retained treatment significantly increased the contents of soluble sugar and starch in seeds from the milk stage to the dough stage and enhanced the activities of SOD, CAT, and POD to maintain redox homeostasis. Transcriptome analysis indicated that differentially expressed genes were significantly enriched in pathways including starch and sucrose metabolism and ascorbate and aldarate metabolism, among which , , , and were identified as key genes regulating seed development, and WGCNA showed that the brown module was significantly correlated with soluble sugars and starch, with hub genes consisting of seven 60S ribosomal proteins and one prolyl 4-hydroxylase. In conclusion, awns positively affect the thousand seed weight of seeds by promoting the synthesis of storage substances, optimizing the antioxidant enzyme system, and regulating the ascorbate and aldarate metabolism pathway and the expression of hub genes. These findings clarify the physiological and molecular mechanisms by which awns regulate seed thousand seed weight and provide a theoretical basis and gene resources for the innovation of high-yield and high-quality germplasms of alpine forage grasses. - Source: PubMed
Publication date: 2026/06/01
Qiu YongsenLu HuanhuanZhao YancuiTang LiubanZhang FeiZhang RuiXie Wengang - 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