TRIM25 _ RNF147 antibody Host rabbit
- Known as:
- TRIM25 _ RNF147 (anti-) Host host: rabbit
- Catalog number:
- 'C11026-2
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- TRIM25 _ RNF147 antibody Host rabbit
Related genes to: TRIM25 _ RNF147 antibody Host rabbit
- 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 _ RNF147 antibody Host rabbit
Related articles to: TRIM25 _ RNF147 antibody Host rabbit
- SARS-CoV-2 3CL protease (3CL) plays crucial role in the viral life cycle by releasing different non-structural proteins from viral polyproteins. It also interacts with several host factors and orchestrates different host cell pathways by cleaving key cellular factors involved in immune modulation, cellular metabolism and cell death. Several host factors have been identified as high confidence substrates of 3CL which regulates host cellular environment both in an enzyme-dependent and enzyme-independent manner. Degradation of RIG-I, TRIM25 and NLRP12 by 3CL downregulates the innate immune response while enzyme-independent interaction with host factors like MAVS promote both its degradation and upregulation. Cellular transcription and translation are altered by interaction of 3CL with host proteins. It affects cell-death by interacting with factors like Gal-8, NDP52 and GSDMD. Post-COVID neurodegenerative disorders have been observed due to the downregulation of neuronal factors like NEMO and UBE3A. The spectrum of 3CL interaction with the key host factors indicates the alternate role of viral protease that modulates host response during infection. Several 3CL targets and their cleavage sites on the target proteins have been identified. This review highlights the crosstalk between 3CL and different host factors as possible alternate therapeutic targets to inhibit the viral propagation as well as address the post COVID clinical issues. - Source: PubMed
Publication date: 2026/06/10
Sanyal DebosmitaChaubey Binay - 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