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)
- Vesicular stomatitis virus is a zoonotic rhabdovirus that infects livestock and can cause economically important disease. Tripartite motif-containing 25 (TRIM25) is an E3 ubiquitin ligase involved in innate antiviral signaling, but its role in pigs during vesicular stomatitis virus infection is unclear. - Source: PubMed
Cao YingZhang JinxiaYoo DongwanZhang HaowenJiang DandanHu YueCong XiaoyanLi JuntongWu XiangjuDu YijunQi JingHuang Juan - Chronic inhalation of crystalline silica precipitates silicosis, a progressive fibrotic lung pathology for which effective therapeutic strategies are currently lacking. Sophoricoside, a bioactive isoflavone glycoside derived from the seeds of Sophora japonica, possesses documented antioxidant and anticoagulant activities; however, its potential antifibrotic efficacy remains ill-defined. Accordingly, the present investigation seeks to systematically evaluate the protective effects of Sophoricoside against pulmonary fibrosis and to decipher the molecular mechanisms governing its action. - Source: PubMed
Publication date: 2026/06/01
Qian JiazhenLi SiyuanDeng LangWang XingchenRen LuHu YanZhou YuxingXie WeixiTang SiyuanZhang LuLi XinLiu YazhuoLiu Wei - Atherosclerosis (AS) is a chronic inflammatory vascular disorder in which endoplasmic reticulum stress (ERS) plays a crucial regulatory role. However, the biological and translational relevance of ERS-related gene networks in AS remains largely unexplored. This study aimed to identify a robust ERS-related gene signature for AS. We integrated multiple GEO datasets and applied machine learning algorithms, including least absolute shrinkage and selection operator (LASSO) regression, support vector machine-recursive feature elimination (SVM-RFE), and random forest (RF). Five ERS-related signature genes (TRIM25, CYBB, CYBA, MYOC, and PRKAA2) were identified and showed favorable discriminatory performance in the integrated discovery cohort (combined AUC = 0.946). The expression patterns of these genes were further examined at both the mRNA and protein levels by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting (WB) in an oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury model. Gene set enrichment analysis and immune infiltration analysis indicated that the identified genes were primarily involved in oxidative stress and immune-related pathways. Collectively, this study identifies a machine learning-derived ERS gene signature associated with AS. These findings improve our understanding of ERS-related vascular injury in AS and provide candidate biomarkers for further tissue-level and mechanistic validation. - Source: PubMed
Publication date: 2026/06/01
Qu XiaomengShao YimingLi HanBao YuhanSun ZhenYu Shuhua - Lung cancer remains one of the most prevalent and deadly malignant neoplasms worldwide, with smoking being a primary risk factor. Among the numerous carcinogens in tobacco smoke, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most potent. The carcinogenic effects of NNK are believed to be mediated through its metabolic activation by CYP2A13 in the lungs, leading to DNA adduct formation and subsequently lung cancer development. However, whether NNK exerts its carcinogenic effects by upregulating CYP2A13 expression and the mechanisms by which NNK upregulates CYP2A13 remain unclear. In this study, we demonstrated that CYP2A13 was overexpressed in human lung adenocarcinoma and NNK exposure significantly upregulated the expression of CYP2A13 in bronchial epithelial cells. Mechanistically, NNK exposure enhanced both transcription and stabilization of CYP2A13 mRNA. Further exploration showed that elevated transcription of CYP2A13 was mediated by the activation of the p-PP2A-C/p-JNK/p-c-Jun signaling axis, while CYP2A13 mRNA stability was driven through the S6/TRIM25/Dicer/miR-7108-3p axis. These findings not only provide critical insights into the mechanisms underlying NNK-induced lung carcinogenesis, but also identify potential therapeutic targets, including PP2A, TRIM25, and miR-7108-3p, for further exploration. - Source: PubMed
Publication date: 2026/05/30
Zhao YunpingWang ZhengZhou ZhihanGe DonghuaiWang JingjingCheng NanYe LiuxianPan ZhihuiChen LiangyuHu LimengLiu XueleiHuang ShiruiLi JingxiaYin LeiXie QipengWang GuiyingHuang Chuanshu - The Nipah virus (NiV) matrix (M) protein, essential for viral assembly, has been increasingly recognized for its potential immunomodulatory functions. However, its role in modulating the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway-a central regulator of inflammation and innate immunity-remains poorly defined. Here, we demonstrate that NiV-M significantly promotes activation of the classical NF-κB pathway. Our data showed that NiV-M interacts with multiple cellular signaling molecules of the NF-κB pathway, including tripartite motif containing 25 (TRIM25), inhibitor of nuclear factor kappa-B kinase subunit alpha (IKKα), nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor alpha (IκBα), and the p65 subunit of NF-κB. Further analyses revealed that NiV-M enhanced the E3 ubiquitin ligase activity of TRIM25, facilitating its interaction with both retinoic acid-inducible gene I (RIG-I) and TNF receptor-associated factor 2 (TRAF2), thereby promoting K63-linked ubiquitination of RIG-I and TRAF2. Moreover, NiV-M strengthened the interaction between IKKα and IKKβ, leading to enhanced IKK complex activity and accelerated degradation of IκBα. In addition, NiV-M promoted phosphorylation and nuclear translocation of p65, thereby amplifying NF-κB-driven gene expression. In summary, our results demonstrate a multifaceted strategy by which NiV-M regulates the NF-κB pathway, a mechanism that may contribute to NiV pathogenesis via inflammatory dysregulation. These findings suggest potential therapeutic approaches for alleviating symptoms associated with immunopathology of NiV by targeting virus-host interactions.IMPORTANCEThis study reveals a previously unknown role of the Nipah virus matrix (M) protein in driving excessive inflammation, a key factor in the virus's high mortality. We discovered that the M protein acts as a master switch, hijacking a central human immune pathway (NF-κB) at multiple points to trigger a "cytokine storm." This explains how the virus causes severe tissue damage and organ failure in infected individuals. By identifying the specific human proteins targeted by the M protein, our work establishes that this viral component functions not only in viral assembly but also in the dysregulation of host inflammatory responses, thereby providing a new perspective on its potential contribution to severe NiV-associated disease. These findings open new avenues for treating NiV infections by developing drugs that target these interactions, potentially controlling the devastating inflammation rather than just the virus itself. - Source: PubMed
Publication date: 2026/05/21
Ye ChangMa XiaoyuKe XianliangYao ZhongziLiu RenyiLi TianZhang PeiluWakjira Bayeta SenbetaTang ShixiangLiu FengYe ZiXie YingChen Quanjiao