Ask about this productRelated genes to: TRIM59 antibody
- Gene:
- TRIM59 NIH gene
- Name:
- tripartite motif containing 59
- Previous symbol:
- TRIM57
- Synonyms:
- TSBF1, Mrf1, RNF104
- Chromosome:
- 3q25.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-12
- Date modifiied:
- 2016-10-05
Related products to: TRIM59 antibody
Related articles to: TRIM59 antibody
- Methyl-CpG binding domain protein 3 (MBD3) functions as a critical tumor suppressor in lung adenocarcinoma (LUAD), yet the ubiquitin-dependent mechanisms orchestrating its proteasomal turnover remain elusive. Here, we demonstrate that MBD3 undergoes ubiquitination and identify tripartite motif-containing protein 59 (TRIM59) as the cognate E3 ligase. TRIM59 physically associates with the N-terminal MBD domain of MBD3 and catalyzes its polyubiquitination and degradation, and mass spectrometry mapping reveals that this process occurs primarily at lysine residues K41, K90, and K92. Functional characterization of the TRIM59-MBD3 axis reveals its role in derepressing the heat shock transcription factors HSF1 and HSF2, thereby driving malignant proliferation and tumor progression. Tissue microarray immunohistochemistry reveals that TRIM59 is upregulated, whereas MBD3 is downregulated in LUAD tissues, establishing an inverse expression pattern that supports oncogenesis. Our findings unveil an unappreciated layer of MBD3 regulation and identify the TRIM59-MBD3 ubiquitination cascade as a potential therapeutic vulnerability in LUAD. - Source: PubMed
Publication date: 2026/01/25
Yang WenhuiRen JinWang YufangShi JiaheCai ZiwanCai CuihongZheng JingQu JingjingZhou Jianya - Spinal cord injury (SCI) is a severe central nervous system disorder for which effective therapeutic interventions remain limited. Accumulating evidence indicates that ferroptosis is a key contributor to secondary neuronal damage following SCI, yet its upstream regulators-particularly those involving post-translational modifications such as ubiquitination-remain incompletely understood. This study aimed to determine whether the E3 ubiquitin ligase TRIM59 modulates neuronal ferroptosis and functional recovery after SCI, and to elucidate its molecular substrate and underlying mechanism of action. - Source: PubMed
Publication date: 2026/03/30
Hu TaoWang WeiZhao XuanCui PengZhang HaojieFan ZuoranWang DongfanHu XinliHuang HaixiaChen XiaolongRong YuluoLu Shibao - As a key tool for assessing aging, DNA methylation clocks are mostly constructed based on European and American populations and rely on the high-cost Infinium MethylationEPIC microarray. These factors limit their widespread application in the Chinese population. - Source: PubMed
Publication date: 2026/04/10
Liu FengLi HaohaoChen TianzheChen XiaoliangHong BoWang HongzhiTu YepingNie Jinfu - Cancer-associated fibroblasts (CAFs) are central to the pancreatic ductal adenocarcinoma (PDAC) microenvironment, promoting tumor progression and therapeutic resistance. However, the expression landscape of CAF membrane proteins in PDAC remains poorly defined. We integrated scRNA-seq (n = 33; 87,949 cells), spatial transcriptomics (n = 2; 7,011 spots), and bulk RNA-seq (n = 7; 642 samples) to systematically identify PDAC-specific CAF membrane genes. A LASSO-based Cox model was developed to construct a prognostic signature, PaFMS, and evaluated through multi-cohort validation. Functional enrichment, immune infiltration, drug sensitivity, and immunotherapy response analyses were further conducted. Validation was performed using multiple database-driven analyses. We identified a PDAC-enriched myoCAF-c1 cluster closely associated with epithelial-mesenchymal transition (EMT) and angiogenesis. From this cluster, 33 candidate CAF membrane genes were defined, whose protein-protein interactions were predominantly linked to extracellular matrix organization and collagen remodeling, and spatially colocalized with myoCAF-c1 and EMT regions. An 11-gene prognostic signature, PaFMS that robustly stratified patients across six independent cohorts, achieving high predictive accuracy for overall survival. High-risk patients exhibited proliferative signaling activation, immune suppression, and reduced T/B-cell infiltration. PaFMS was associated with responses to 33 anticancer agents and predicted enhanced benefit from anti-PD-L1 immunotherapy in the low-risk group. Multi-cohort validation confirmed the expression specificity of PaFMS genes, including PLAU, TMEM158, and TRIM59. Together, these findings reveal that myoCAF-c1 promotes angiogenesis and tumor progression, and establish PaFMS as a robust CAF membrane-based prognostic model in PDAC with potential utility for precision prognosis and therapeutic decision-making. KEY MESSAGES: Integrated single-cell, spatial, and bulk RNA-seq analyses identified PDAC-specific CAF membrane genes. Discovered a PDAC-enriched myoCAF-c1 subtype linked to EMT and angiogenesis. Developed an 11-gene CAF membrane-based prognostic model (PaFMS) validated across six cohorts. PaFMS predicts patient survival, drug sensitivity, and immunotherapy response in PDAC. - Source: PubMed
Publication date: 2026/04/06
Zhuang LeshiZhang WeiWu JunCao JianFeng LiangCao Shubo - Gastric cancer (GC) is among the most common malignant tumors worldwide. The inhibition of p53 ubiquitination can inhibit the progression of GC. The mechanism through which plasmolipin (PLLP) regulates p53 ubiquitination in GC remains unclear. In this study, the correlation between PLLP expression and the prognosis of GC was analyzed on the basis of data from The Cancer Genome Atlas database, and the expression characteristics of PLLP and p53 were verified by immunohistochemistry. A PLLP overexpression/knockdown GC cell model was constructed, and cell proliferation, apoptosis, and invasion were detected by Cell Counting Kit-8, flow cytometry, and Transwell assays. Coimmunoprecipitation and Western blotting were used to analyze the PLLP-tripartite motif-containing 59 (TRIM59)-p53 regulatory axis. The antitumor effect of PLLP in vivo was verified by tumor formation experiments in nude mice. Cycloheximide tracking assays, coimmunoprecipitation, and ubiquitination analysis were used to determine the effect of PLLP on p53 stability. Combined with bioinformatics prediction and experimental verification, the interaction between PLLP and the E3 ubiquitin ligase TRIM59 and its regulatory effect on the ubiquitination and degradation of p53 were analyzed. Flow cytometry and Transwell assays were used to verify the biological effect of the PLLP-TRIM59-p53 axis. We found that PLLP was downregulated in GC (p < 0.05). PLLP interacts with TRIM59, inhibits TRIM59-mediated ubiquitination degradation of p53, and inhibits the progression of GC cells with WT p53. PLLP may be used as a potential biomarker for targeted therapy of GC. - Source: PubMed
Publication date: 2026/03/04
Quan ZhenhaoLin LinXu FeipengZhou CaijinHuang RenweiSun KaiyuJiang Haiping