Ask about this productRelated genes to: UBE4A antibody
- Gene:
- UBE4A NIH gene
- Name:
- ubiquitination factor E4A
- Previous symbol:
- -
- Synonyms:
- UBOX2, UFD2, KIAA0126, E4
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-28
- Date modifiied:
- 2016-11-09
Related products to: UBE4A antibody
Related articles to: UBE4A antibody
- - Source: PubMed
Zhang Ming-PengSong ZaozhiZhang Wei-SanTan JinZhao Ming-HuiLian Lin-JuanCai Jie - There is compelling evidence that TNF preferentially activates and expands CD4Foxp3 regulatory T cells (Tregs) through TNFR2. However, the precise mechanisms underlying TNF-TNFR2 pathway-mediated Treg proliferation remain to be fully elucidated. In this study, using RNA-seq profiling of TNFR2 and TNFR2-deficient Treg cells, we identified that Trip13 is required for promoting TNF-TNFR2 pathway-mediated Treg expansion. Mechanistically, TRIP13 inhibited UBE4A-mediated ubiquitination degradation of HAT1 by directly binding to HAT1, thereby competing with UBE4A and promoting Treg expansion. In addition, TRIP13's ATPase activity was essential for its binding to HAT1, which promoted Treg expansion by increasing Foxp3 expression. In a mouse colitis model, TRIP13 overexpression markedly alleviated colon inflammation by enhancing Treg expansion, an effect that was reversed by HAT1 knockdown. Conversely, genetic ablation of TRIP13 substantially reversed the effects induced by HAT1 overexpression, including enhanced Treg expansion and attenuation of colitis. These findings illustrate the TRIP13/HAT1 axis-mediated mechanism for TNF-TNFR2-induced Treg expansion and indicate that targeting TRIP13 may offer therapeutic potential for autoimmune and inflammatory diseases. - Source: PubMed
Publication date: 2026/01/14
He TianzhenZhao LiwenFeng Chu-TingZhao Li-YaJing ShengnanYang HanWang KeYe SiyuZhao YingchunYu YingFu ZhutingChou Chon-KitChen XinGao Yong-Jing - Ubiquitin-dependent signaling is essential for maintaining intestinal homeostasis and its dysregulation contributes to chronic intestinal disorders, such as Inflammatory Bowel Disease (IBD). Ube4A is a U-box E3/E4 ubiquitin ligase involved in lipid metabolism and insulin signaling in metabolic tissues. Autoantibodies against Ube4A have been identified in patients with IBD and are associated with disease long-term complications. Despite these clinical associations, the physiological role of Ube4A in the gastrointestinal tract remains unknown. This study aimed to define the function of Ube4A in the colon and determine how its loss influences susceptibility to experimental colitis. - Source: PubMed
Publication date: 2026/01/03
Guignard SimonChakraborty MoleeGonzalez-Nieves SilviaDeBruin DavidEbert EmilyVinogradskaia AnastasiiaBrennan MichelleTeague Ryan MChakraborty AnutoshCifarelli Vincenza - Osteosarcoma (OS) is the most common primary bone tumor. Insulin Growth Factor-2 Binding Protein 3 (IGF2BP3) regulates mRNA stability and is a potential oncogene in many cancers, but its role in OS remains unknown. - Source: PubMed
Publication date: 2025/08/14
Li ShuoWang TianyangWang ErjianLin LinZhong Wei - Coxsackievirus B3 (CVB3)-induced acute heart failure (AHF) is a common cause of cardiogenic death in young- and middle-aged people. However, the key molecular events linking CVB3 to AHF remain largely unknown, resulting in a lack of targeted therapy strategies thus far. Here, we unexpectedly found that Viperin deficiency does not promote CVB3 infection but protects mice from CVB3-induced AHF. Importantly, cardiac-specific expression of Viperin can induce cardiac dysfunction. Mechanistically, CVB3-encoded 3C protease rescues Viperin protein expression in cardiomyocytes by lowering UBE4A. Viperin in turn interacts with and reduces STAT1 to activate SGK1-KCNQ1 signaling, and eventually leads to cardiac electrical dysfunction and subsequent AHF. Furthermore, we designed an interfering peptide VS-IP1, which blocked Viperin-mediated STAT1 degradation and therefore prevented CVB3-induced AHF. This study established the first signaling link between CVB3 and cardiac electrical dysfunction, and revealed the potential of interfering peptides targeting Viperin for the treatment of CVB3-induced AHF. - Source: PubMed
Publication date: 2025/04/08
Yuan YukangQian LipingMiao YingCui QunCao TingYu YongZhang TingtingZhao QianZhang RenxiaRen TengfeiZuo YiboDu QianQiao CaixiaWu QiuyuZheng ZhijinLi MinqiChinn Y EugeneXu WeiPeng TianqingChen RuizhenXiong SidongZheng Hui