TRIM31 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- TRIM31 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100142
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- TRIM31 antibody Polyclonal Antibodies Primary antibodies
Related genes to: TRIM31 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- TRIM31 NIH gene
- Name:
- tripartite motif containing 31
- Previous symbol:
- -
- Synonyms:
- RNF, HCGI, C6orf13, HCG1
- Chromosome:
- 6p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-16
- Date modifiied:
- 2016-10-05
Related products to: TRIM31 antibody Polyclonal Antibodies Primary antibodies
Related articles to: TRIM31 antibody Polyclonal Antibodies Primary antibodies
- Esophageal squamous cell carcinoma (ESCC) is among the most lethal malignancies worldwide, with a five-year survival rate below 20%. Ferroptosis-a regulated form of cell death driven by iron-dependent lipid peroxidation-has emerged as a promising therapeutic strategy, yet its regulation in ESCC remains poorly understood. We investigated the role of tripartite motif-containing 31 (TRIM31), an E3 ubiquitin ligase, in ESCC progression and ferroptosis. - Source: PubMed
Publication date: 2026/01/11
Wang ZeChang KejieZhang KeWang PeiBai GuangjianWang ZhenhuaXiao JianTong XinZhao Jun - Lung cancer (LC) causes large amount of cancer death worldwide. As the most common and aggressive type of LC, the molecular mechanisms in LUAD (Lung Adenocarcinoma) remain unclear. In order to find novel potential molecular targets for improving the prognosis of LUAD, we obtained gene information of LUAD patients from The Cancer Genome Atlas (TCGA) and identified hub genes through weighted gene co-expression network analysis (WGCNA). We selected the top 25% of total 5945 differently expressed genes (DEGs) and established 16 modules. The purple module was highly associated with tumor stage and chosen as key module. Further analysis revealed that the level of 6 hub genes (TRIM31, DKK1, FAM83A, RHOV, S100P and TSKU) were negatively relevant to survival rate but positively correlated with advanced tumor stage. Immunohistochemistry (IHC), western blot (WB) and reverse transcription-quantitative PCR (RT-qPCR) verified the high expression of TRIM31 in LUAD. Loss-of-function assays indicated TRIM31 accelerated viability, proliferation and metastasis of LUAD cells. According to the UbiBrowser website, TRIM31, as an E3 ubiquitin ligase, may be involved in the ubiquitination of P53, an important tumor suppressor. Co-immunoprecipitation verified the interaction between TRIM31 and P53. More importantly, the degradation rate of P53 was slowed when TRIM31 was knockdown. Further immunoblot assays revealed that TRIM31 promoted the ubiquitination and degradation of P53. P53 could inhibit the expression of SLC7A11 and was regarded as an important regulator of ferroptosis. Ferroptosis analysis showed that TRIM31 knockdown decreased cell viability and GSH, but increased ROS, MDA and iron, which could reverse by knockdown of P53. Above results displayed that TRIM31 effected ferroptosis level via P53. In addition, website prediction showed that BATF was a transcription factor of TRIM31, and experiments confirmed that BATF could indeed promote the transcription of TRIM31. Taken together, the data demonstrated that TRIM31 promoted LUAD progression by inhibiting ferroptosis via the TRIM31/P53/SLC7A11 axis. - Source: PubMed
Publication date: 2026/03/26
Dou TingtingLiu YanminFang XiaochangYang LijieShu LinChen TianliangYang TiechengYin YilinWang HuaqiaoFeng MaohuiLi Xuanfei - Idiopathic pulmonary fibrosis (IPF) is a serious and progressive lung disease characterized by devastating and progressive fibrosis. Treatment is unsatisfactory. There is accumulating evidence that transplantation of mesenchymal stem cell derived exosomes (MSC-EXOs) protects against IPF. This study aimed to investigate the protective effects of EXOs isolated from human induced pluripotent stem cell-derived MSCs (iPSC-MSC-EXOs) on pulmonary fibrosis and explore the underlying mechanisms. Exosomes were isolated from bone marrow-MSCs (BM-MSCs) and iPSC-MSCs and subsequently identified. A mouse model of pulmonary fibrosis was established by tracheal injection of bleomycin (BLM) followed by transplantation of BM-MSC-EXOs or iPSC-MSC-EXOs via tail vein injection. Pulmonary function and fibrosis were assessed by pulmonary function tests (PFT) and Masson trichrome staining, respectively. Mice lung fibroblasts (LFs) were treated with BM-MSC-EXOs or iPSC-MSC-EXOs in the presence of TGF-β1 in vitro. Compared with BM-MSC-EXOs, iPSC-MSC-EXO treatment significantly enhanced pulmonary function and decreased the fibrosis and lactate level in a mouse model of BLM-induced pulmonary fibrosis. In vitro, iPSC-MSC-EXOs exerted a superior protective efficacy against TGF-β1-induced LF activation via downregulation of the lactate level. Further analysis revealed a higher protein level of TRIM31 in iPSC-MSC-EXOs than BM-MSC-EXOs. Mechanistically, exosomal TRIM31 from iPSC-MSC-EXOs inhibited LF activation via downregulation of glycolysis by mediating ubiquitination of hexokinase 2 (HK2). Furthermore, knockdown of TRIM31 reduced the protective effects of iPSC-MSC-EXOs on pulmonary fibrosis in BLM-treated mice. Our study showed that TRIM31 delivered by iPSC-MSC-EXOs exerted anti-pulmonary fibrotic effects by alleviating LF activation via regulation of HK2 ubiquitination. This study provides a potential therapeutic strategy for patients with IPF. - Source: PubMed
Publication date: 2026/01/28
Li ZiqiLiang XiaotingGuo BingpengMao MengmengWang ShuchangYang QiZhao JunxiuLin FangMa KexinHu BeiHan QianZhang Yuelin - Mitochondrial dysfunction is closely associated with the pathogenesis of Parkinson's disease (PD). Lutein has been shown to exert protective effects in neurological disorders. This study aimed to investigate the ameliorative effects of lutein on mitochondrial function in PD and its underlying molecular mechanisms. - Source: PubMed
Duan JiabinDuan WenbinPu XiaominMa ChangdiHuang HuaiXu Zhenghu - The activation of NLRP3 inflammasome contributes to the development of numerous chronic inflammatory diseases, including ulcerative colitis and stress-induced anxiety. Recent studies have revealed that NLRP3 K48-linked ubiquitination by several E3 ligases, including Trim31, leads to degradation. Neddylation is a process highly similar to ubiquitination by covalently conjugating NEDD8 to lysines in specific substrate proteins. Neddylation of substrate proteins alters their subcellular localization, stability, and activity. The role of neddylation in the NLRP3 inflammasome remains elusive. Here, we report that neddylation promotes the activation of the NLRP3 inflammasome in macrophages. Myeloid deficiency of UBA3, the catalytic subunit of the NEDD8-activating enzyme (NAE), renders mice resistant to dextran sodium sulfate-induced colitis. Inducible Uba3 deletion in microglia mitigates psychological stress-induced anxiety-like behavior. Neddylation blockade led to a reduced protein level of NLRP3 without affecting its mRNA level. Further exploration revealed that NLRP3 undergoes neddylation at K287 with Ube2M as the E2 and Smurf2 as an E3, respectively. NLRP3 neddylation hinders its interaction with Trim31 and thereby inhibits its K48-linked ubiquitination and subsequent degradation. MLN4924, a potent compound NAE inhibitor in phase 1/2/3 clinical trials for cancers, alleviates psychological stress-induced NLRP3 inflammasome activation, microglia inflammatory activation, and anxiety-like behavior, suggesting novel clinical activity of MLN4924. - Source: PubMed
Publication date: 2026/01/09
Gai WenbinWu MengyaoWu AnbiaoJing ZhaofeiYe ZhenjieJin JiayanZhang YaolinZhao MinLiu GenyuWang XuYang XiqinDong JieXu YunluZhang Jiyan