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)
- To characterize shared immune-associated programs between sepsis and systemic lupus erythematosus (SLE), define the cellular context of prioritized candidate genes, and functionally evaluate SIGLEC1 in macrophage inflammatory responses. - Source: PubMed
Publication date: 2026/09/03
Xu YanWang HaoHu YingchunLan Youyu - Guanylate-binding protein 2 (GBP2) has been reported to be involved in the progression of various human malignancies, but its specific functions and underlying molecular mechanisms in pancreatic cancer remain poorly understood. - Source: PubMed
Publication date: 2026/08/17
Fang ShilinNie HaihangZhou JingkaiZhang YongxiLiu XiaopingGuo JianchunHong YuntianDing YangNing YumeiWang FanKe HengningFang JunWang Haizhou - Goose astrovirus (GAstV) is an important pathogen associated with visceral gout, growth retardation, and mortality in goslings, whereas the splenic response to infection remains poorly understood. In this study, GAstV-infected goslings showed positive viral RNA detection in spleen tissues, obvious splenomegaly, and histopathological lesions. Transcriptomic analysis identified 383 differentially expressed genes, including 243 upregulated and 140 downregulated genes. Functional enrichment analyses showed that these genes were mainly involved in antiviral defense, innate immune responses, complement and coagulation cascades, and the RIG-I-like receptor signaling pathway. GSEA further supported the enrichment of the RIG-I-like receptor signaling pathway in infected spleens. Notably, several genes related to this pathway, including , , , and , were markedly upregulated and were also identified as hub genes in the protein-protein interaction network. RT-qPCR validation further confirmed the upregulation of these hub genes in GAstV-infected spleens, corroborating the transcriptomic findings. Collectively, these findings indicate that GAstV infection is associated with splenic lesions and extensive transcriptional reprogramming in goslings, and suggest that RIG-I-like receptor-related antiviral signaling may be involved in the splenic innate immune response to GAstV infection. This study provides new transcriptomic insight into the innate immune responses associated with GAstV infection. - Source: PubMed
Publication date: 2026/08/26
Peng GuangzhongGuo XinranGu YingjieFan SuyuHu XumingZhang YangChen GuohongZhao WenmingXu Qi - The mycobacterial ESX-1 (Type VII) secretion system is essential for virulence and induces the NLRP3 inflammasome activation. However, the specific bacterial effectors involved in this process, beyond the well-characterized EsxA (ESAT-6), remain largely unidentified. Through systematic screening of ESX-1 effectors, we identified EspF as a potent and evolutionarily conserved activator of the NLRP3 inflammasome across pathogenic mycobacterial species, including , , and . Our results demonstrate that EspF significantly augments the mature IL-1β and IL-18 release, ASC speck formation, caspase-1 activation, and gasdermin D (GSDMD)-mediated pyroptosis in THP-1 cells. Notably, infection with or BCG strain overexpressing EspF significantly enhanced NLRP3 inflammasome activation and pyroptosis, which were completely abolished in NLRP3-deficient cells. Mechanistically, EspF directly interacts with the NACHT and LRR domains of NLRP3. Furthermore, unbiased proteomic screening identified the host E3 ubiquitin ligase TRIM25 as an indispensable binding partner. In THP-1 cells, we confirmed the endogenous interaction and colocalization of the EspF-TRIM25-NLRP3 complex, demonstrating that EspF functions as a molecular scaffold that bridges TRIM25 to NLRP3. This proximity interaction, further validated during mycobacterial infection, facilitates TRIM25-mediated K63-linked ubiquitination of NLRP3. , mice infected with BCG strains overexpressing EspF exhibited exacerbated lung lesions, increased inflammatory cell infiltration, and higher bacterial burdens. Collectively, these findings reveal EspF-TRIM25-NLRP3 axis is a novel mechanism of mycobacterial pathogenesis that drives hyperinflammation to facilitate bacterial survival and dissemination. - Source: PubMed
Publication date: 2026/09/08
Yang YangHan YixinWu LongjianZang XinxinXu WeiLi YunjieXu AhuiJiang HexiangFan JingyanCui LuqingHuang BeiHe GuiqingSong Houhui - Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality, yet mechanisms sustaining malignant progression remain incompletely defined. Integrative analyses across multiple HCC cohorts identified TUBA1B as one of the most consistently upregulated tubulin isotypes whose high expression associates with poor prognosis and metastasis. In hydrodynamic tail-vein injection (HTVi) models, co-expression of Tuba1b with myr-AKT enhanced liver tumor growth, supporting a tumor-promoting role for Tuba1b in vivo. TUBA1B knockdown suppressed HCC cell proliferation, migration, and invasion in vitro and reduced tumor growth and metastasis in orthotopic models. HTVi-mediated delivery of sgTuba1b suppressed hepatocarcinogenesis in NRasV12/myr-AKT- and MYC/sg-p53 HCC models and prolonged survival in the former, whereas sgTuba1b delivery to normal livers caused no detectable histological abnormalities. Mechanistically, TUBA1B bound and stabilized G3BP2 by restraining TRIM25-dependent K48-linked ubiquitination, thereby promoting G3BP2-IκBα association and sustaining basal NF-κB/p65 transcriptional activity; enforced G3BP2 expression rescued the proliferative and metastatic defects caused by TUBA1B loss. Clinically, combined upregulation of TUBA1B and G3BP2 with elevated p65 activity delineated a high-risk HCC subgroup with the poorest outcomes. Collectively, these findings define a TUBA1B-G3BP2 stability axis that supports malignant phenotypes and highlight a potential therapeutic vulnerability in HCC. - Source: PubMed
Publication date: 2026/09/06
Lin FenLin HechunYu JunmingGe ChaoMao LinZhang SaihuaJin YiziWu YunyuChen TaoyangLi JinjunLi Hong