TRIM25 Antibody (monoclonal) (M02)
- Known as:
- TRIM25 Antibody (mab) (M02)
- Catalog number:
- AT4346a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- TRIM25 Antibody (monoclonal) (M02)
Related genes to: TRIM25 Antibody (monoclonal) (M02)
- Gene:
- EMC10 NIH gene
- Name:
- ER membrane protein complex subunit 10
- Previous symbol:
- C19orf63
- Synonyms:
- INM02, HSS1, HSM1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-17
- Date modifiied:
- 2016-12-01
- Gene:
- MRPL1 NIH gene
- Name:
- mitochondrial ribosomal protein L1
- Previous symbol:
- -
- Synonyms:
- BM022
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2015-08-25
- Gene:
- PMS2 NIH gene
- Name:
- PMS1 homolog 2, mismatch repair system component
- Previous symbol:
- PMSL2
- Synonyms:
- H_DJ0042M02.9, HNPCC4, MLH4
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
- Gene:
- SESN2 NIH gene
- Name:
- sestrin 2
- Previous symbol:
- -
- Synonyms:
- SES2, DKFZp761M0212, HI95, SEST2
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2016-10-05
- Gene:
- TRIM25 NIH gene
- Name:
- tripartite motif containing 25
- Previous symbol:
- ZNF147
- Synonyms:
- EFP, RNF147
- Chromosome:
- 17q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-16
- Date modifiied:
- 2015-09-01
Related products to: TRIM25 Antibody (monoclonal) (M02)
Related articles to: TRIM25 Antibody (monoclonal) (M02)
- The pathology of intervertebral disc degeneration (IDD) is characterized by metabolic dysregulation within nucleus pulposus (NP) cells. TRIM25 has been implicated in diverse tumors and pathological processes, yet its precise role in mediating mitochondrial function and metabolic alterations during IDD progression remains unclear. - Source: PubMed
Liu XiaomingZhang WenyuFeng HangLai LinyingCao ChenYang GuangGao YanzhengWang BijunWang HuiYu BinYu Zhenghong - The red-spotted grouper nervous necrosis virus (RGNNV) exhibits high pathogenicity in larval , yet the immune molecular mechanism remains unclear. Non-coding RNAs (ncRNAs) are vital in the host's immune responses during viral infection. However, there has been no study on ncRNA research for this species to date. We systematically identified 105 DE microRNAs (miRNAs), 157 DE long non-coding RNAs (lncRNAs) and 31 DE circular RNAs between the infection group and control group. Functional enrichment analysis revealed that these differentially expressed genes were significantly enriched in pathways associated with innate immune defense, inflammatory, and cell death, such as JAK-STAT signaling pathway, NF-κB signaling pathway, apoptosis, and necroptosis. Furthermore, the lncRNA-miRNA-mRNA interaction network involving miR-93 was constructed, which may represent a promising candidate therapy target for future investigations. This study presents the first comprehensive ncRNA transcriptome dataset of infected with RGNNV, identifies key antiviral defense and cell death-related genes and hub pathways, and thereby identifies miR-93-involved lncRNA-miRNA-mRNA network and key targeted genes () as hub molecular regulators in immune response of this species. - Source: PubMed
Publication date: 2026/08/12
Guo XiaoliGao ChengbinChen ZhangfanLu ShengWang LeiLi WenshengHe XinleiYang ChuanjunLi JianweiChen Songlin - Efficient transgene expression following nucleic acid transfection remains difficult in many fish cell lines, particularly those derived from marine species. Although extracellular delivery systems have been extensively optimized, intracellular factors that limit the expression of delivered nucleic acids remain poorly understood in teleosts. In mammals, TRIM25 (tripartite motif-containing protein 25) participates in cytoplasmic exogenous RNA surveillance. Here, we examined whether its teleost homolog contributes to the low reporter expression observed after transfection. Transient siRNA-mediated knockdown of trim25 increased the percentage of eGFP-positive cells following Cap1-m¹Ψ-eGFP mRNA transfection from 19.27% to 74.63% in zebrafish embryonic fibroblast cell line (PAC2) and from 10.41% to 36.15% in Chinese tongue sole testis cell line (CST). Reporter expression following pEGFP-N1 plasmid transfection was also increased, although to a lesser extent. In this study, transfection efficiency was operationally defined as the percentage of eGFP-positive cells among total nuclei and did not directly measure nucleic acid uptake. These findings suggest that transient trim25 knockdown may alleviate intracellular restriction of exogenous reporter expression in PAC2 and CST cells and may provide an affordable approach for improving molecular manipulation in selected fish cell systems. - Source: PubMed
Publication date: 2026/08/25
Wang YajunGe XiaohuanGuo TiangeDu MengdaHe Yan - Tumor metastasis remains the leading cause of postoperative recurrence and mortality in patients with clear cell renal cell carcinoma (ccRCC). Although aberrant glucuronic acid metabolism and O-GlcNAcylation are closely associated with tumor progression, the mechanism by which these pathways intersect to regulate ccRCC metastasis remains poorly understood. Here, an orthotopic ccRCC mouse model coupled with comparative proteomic analysis of primary and metastatic lesions identified UDP-glucose-6-dehydrogenase (UGDH) as a pivotal suppressor of metastasis in ccRCC. In vitro and in vivo functional assays confirmed that UGDH overexpression markedly suppressed the invasion and migration of ccRCC cells. Mechanistically, we demonstrated that the E3 ubiquitin ligase TRIM25 facilitates UGDH degradation via K48-linked polyubiquitination, whereas UGDH modulates the expression of tight junction protein 1 (TJP1) via O-GlcNAcylation. Notably, pharmacological inhibition of O-GlcNAcylation with OSMI-1 effectively impeded metastasis in both cellular and animal models. This study reveals a novel tumor-suppressive role for UGDH and highlights the potential of the TRIM25-UGDH-TJP1 axis for diagnostic and therapeutic strategies in metastatic ccRCC. - Source: PubMed
Publication date: 2026/08/19
Chen XiaolinBao YuhangLiu TaoQiu JianhuiMa YuanyuanZhang ZedanWang ChuandongDeng RuiyiSong ZhengHe TianyiLiu HaodeZhou JingchengWang YizhouGong Kan - Among the intracellular sensors of innate immunity against infection, RIG-I-like receptors (RLRs) serve as cytosolic surveillance sensors that detect viral RNA species. However, the role of kinases in modulating RIG-I in a catalytically-independent manner is not well known. In this study, we report that protein kinase DYRK1B is a novel positive regulator of RIG-I-mediated antiviral innate immunity. Overexpression of DYRK1B markedly amplified RNA virus-induced IFN-I production, whereas CRISPR-mediated knockout of DYRK1B substantially attenuated these antiviral responses. Mechanistic investigation revealed that this regulatory role operates independently of DYRK1B's catalytic kinase function; instead, DYRK1B functions as an adaptor protein that connects TRIM25 with RIG-I, thereby promoting TRIM25-mediated K63-linked polyubiquitination of RIG-I, an essential modification required for RIG-I functional activation. Collectively, our findings reveal that DYRK1B enhances innate immunity against RNA viruses by strengthening the physical association of RIG-I with TRIM25, providing a more profound understanding of the mechanisms involved in antiviral immune regulation. - Source: PubMed
Publication date: 2026/08/10
Zeng XianhuangXie JiaYousaf TanzeelNaz WajeehaNing JieZhang ZelinXu YueWu Chao