Ask about this productRelated genes to: TRIM58 antibody
- Gene:
- TRIM58 NIH gene
- Name:
- tripartite motif containing 58
- Previous symbol:
- -
- Synonyms:
- BIA2
- Chromosome:
- 1q44
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-17
- Date modifiied:
- 2015-08-26
Related products to: TRIM58 antibody
Related articles to: TRIM58 antibody
- Thyroid cancer frequently undergoes dedifferentiation, progressing into poorly differentiated or anaplastic carcinoma, which is characterized by therapeutic resistance and a poor prognosis. Epigenetic dysregulation, particularly histone methylation, plays a critical role in this process. In this study, we identify PRDM16 as an essential regulator of thyroid cancer differentiation. Mechanistically, we demonstrate that PRDM16 catalyzes H3K9 monomethylation at the TRIM58 promoter region, thereby enhancing TRIM58 transcription. Upregulated TRIM58 subsequently promotes ubiquitination and degradation of MVP, leading to suppression of both the MAPK and PI3K/AKT signaling pathways and maintenance of cellular differentiation. This PRDM16-TRIM58-MVP axis modulates proliferation, epithelial-mesenchymal transition, and radioiodine uptake in thyroid cancer cells. Moreover, PRDM16 overexpression enhances the efficacy of MAPK inhibitor-induced redifferentiation therapy. Collectively, these findings establish PRDM16 as a novel tumor suppressor and potential therapeutic target, offering a promising redifferentiation-based strategy for the treatment of advanced thyroid cancer. - Source: PubMed
Publication date: 2026/04/23
Yu JialongLuo WeiNiu ZijieZhang MiaoGao YunqiTian MengranWang ZhongyuWan XingGui HanSu QianChen WenhaoHu LinfeiHou XiukunDong QimanRuan XianhuiZheng Xiangqian - Systemic lupus erythematosus (SLE) is a chronic autoimmune disease influenced by multiple genetic and environmental factors.. This study used bioinformatics to identify new diagnostic biomarkers and explore the pathogenesis of SLE. - Source: PubMed
Publication date: 2026/05/11
Pan QingboYu XuliangZhu JinZheng Xiaojin - Innate immune sensors rely on ubiquitin ligases to calibrate antiviral responses, yet the rules governing substrate recognition by SPRY-containing ligases remain poorly defined. Here, we establish a large-scale structure-based screening pipeline using AlphaFold to systematically predict interactions between human nucleic acid sensors and SPRY-containing proteins. Our approach uncovered novel transient or degradation-sensitive interactions that are typically missed by proteomic methods, including a labile TRIM58-OAS1 complex. We show that SPRY domains dictate substrate specificity: TRIM25 preferentially engages ZAP, whereas Riplet favors RIG-I. Domain-swapping experiments demonstrated that SPRY domains are sufficient to reprogram ligase specificity and antiviral activity. Phylogenetic and structural analyses revealed that TRIM25 and Riplet evolved from a common ancestor but diverged in coiled-coil architecture and oligomeric state, while retaining conserved substrate preferences. Residue-level modeling identified hypervariable SPRY loops as critical determinants of recognition, a prediction validated by targeted mutagenesis of the TRIM25-ZAP interface. Finally, we show that distinct SPRY-containing ligases surveil self-amplifying RNA (saRNA) vaccines: Riplet-RIG-I primarily responds when RNA is delivered by lipofection, whereas TRIM25-ZAP is engaged upon lipid nanoparticle delivery, with functional consequences for vaccine expression. Together, these findings demonstrate that SPRY domains encode recognition logic for ubiquitin ligases, that AlphaFold enables discovery of otherwise hidden interactions and that these principles have direct implications for RNA-based therapeutics. - Source: PubMed
Publication date: 2026/05/08
Syed IbrahimChen ShengPeeler David JMcKay Paul FBriones-Orta Marco ABohn Jennifer AShattock Robin JGonçalves-Carneiro Daniel - Lung squamous cell carcinoma (LUSC) remains a therapeutic challenge with limited biomarkers. The tumor immune microenvironment (TIME) is crucial for progression and immunotherapy response. Because SSX1 and TRIM58 emerged as significant independent prognostic factors, this study investigated their combined prognostic and immunological significance in LUSC. - Source: PubMed
Publication date: 2026/04/24
Zhao XiaolingLiu ChengyuSun JiawenWang ChengchengShen QiZhang XiaochongLiu DandanXie JingYang XuLiu Dengxiang - As the most abundant human cell and the foundation of transfusion medicine, red blood cells (RBCs) offer a unique readout of systemic health, yet they have never been characterized at population scale. We generated a proteome atlas of 13,091 blood donors with multi-omics longitudinal phenotyping, characterizing the influence of demographics and genetic variation on the reproducibility of RBC proteomes across donations. Elastic-net aging clocks captured biological aging with high accuracy and uncovered genetic regulators of ΔAge at FN1, C4/IKZF1, CRAT, PFAS, TRIM58. Across independent cohorts, ΔAge was accelerated in G6PD deficiency, sickle cell trait/disease, and iron deficiency, reversed by iron repletion, and slowed in high-frequency donors, linking molecular aging to brain iron/myelin and cognitive performance. Molecular aging signatures predicted storage, osmotic, and oxidative hemolysis, hemoglobin increments after transfusion, and long-term donor activity over 12-years. These results establish RBC proteomics as a scalable biomarker of aging, donor healthspan, and transfusion outcomes. - Source: PubMed
Publication date: 2026/03/08
Dzieciatkowska MonikaIssaian Aaron VKeele Gregory RSaviola AnthonyStephenson DanielBevers ShaunReisz Julie AHaiman Zachary BNemkov TravisFang FangMoore Amy LDeng XutaoStone MarsKleinman SteveNorris Philip JWang XundeThein Swee-LayHod Eldad ABusch Michael PRoubinian Nareg HPage Grier PHansen Kirk CD'Alessandro Angelo