Ask about this productRelated genes to: TRIM45 antibody
- Gene:
- TRIM45 NIH gene
- Name:
- tripartite motif containing 45
- Previous symbol:
- -
- Synonyms:
- FLJ13181, RNF99
- Chromosome:
- 1p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-03
- Date modifiied:
- 2014-11-19
Related products to: TRIM45 antibody
Related articles to: TRIM45 antibody
- This study investigates the protective effect of GB against cerebral I/R injury and explores its underlying mechanism involving the TRIM45- TAB2-TAK1-TAB1 axis. - Source: PubMed
Publication date: 2026/03/30
Lv ZhiyangJi ZhipingChen JingLong TianningNiu HongyunFu PeinanLu MengHao XiaobeiYang Yuwei - Blood and meat spots (BMS) are common internal defects in chicken eggs that compromise egg quality. To reveal genes contribute to BMS formation, we performed an Adaptive Lasso-based genome-wide association study (ALGWAS) of Rhode Island Red (RIR) hens. The results showed that the heritability of BMS was 0.13. Based on ALGWAS, we identified one significant and 144 suggestive SNPs associated with BMS. Within the significant locus, eight candidate genes were annotated (TNFRSF1A, CECR1, TRIM45, CALD1, SIDT1, VTCN1, USF3, ATP6V1A). Among these, VTCN1 emerged as the strongest candidate, supported by eQTL annotation and its established function as an immune checkpoint regulator that modulates inflammation, vascular integrity, and T-cell responses. - Source: PubMed
Publication date: 2026/02/17
Ma XiaolongChen XingCheng XueLiu WeiNing Zhonghua - Cerebral ischemia-reperfusion (I/R) injury is the main cause of early complications and adverse outcomes after treatment such as myocardial infarction and acute ischemic stroke. In this study, we aimed to explore the functions of insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) and tripartite motif-containing 45 (TRIM45) in neuron injury after cerebral I/R injury. HMC3 cells were exposed to oxygen-glucose deprivation and reoxygenation (OGD/R) to mimic cerebral I/R injury in vitro. Western blot and qRT-PCR were conducted for gene expression. NLR family pyrin domain containing 3 (NLRP3) inflammasome activity was analyzed by western blot. ELISA kits were utilized to determine the concentrations of inflammatory cytokines. Flow cytometry was used to analyze iNOS cells, CD206 cells and neuron apoptosis. Methylated RNA Immunoprecipitation (meRIP) assay and RIP assay were adopted to analyze the relation between TRIM45 and IGF2BP1. CCK-8 assay and TUNEL assay were adopted for the viability and death of neurons. Mice model of middle cerebral artery occlusion (MCAO) was used to explore the function of IGF2BP2 in cerebral I/R injury. IGF2BP1 level was upregulated in HMC3 cells. IGF2BP1 overexpression promoted NLRP3 inflammasome activation and pro-inflammatory phenotype in OGD/R-stimulated HMC3 cells. Mechanically, IGF2BP1 modulated TRIM45 expression through m6A methylation modification. IGF2BP1 knockdown inhibited NLRP3 inflammasome activation and pro-inflammatory phenotype in OGD/R-stimulated HMC3 cells by m6A methylation modification of TRIM45. Inhibition of IGF2BP1 improved the viability and suppressed the death and apoptosis of neurons in the co-culture system of microglia-like and neurons by regulating TRIM45 expression. Inhibition of IGF2BP1 improved the neurotoxicity of proinflammatory HMC3 cells in co-cultured neurons via reducing the m6A methylation of TRIM45. However, the number of biological replicate samples was relatively small (n = 3) and the results in this study were preliminary study. - Source: PubMed
Publication date: 2026/02/05
Wang PeiHuang YanlingMa QianZhou YueqinWang XuefeiYang LiuMeng Tao - Bovine leukemia virus (BLV), a member of the Deltaretrovirus genus, causes enzootic bovine leukosis, leading to clinical outcomes that range from asymptomatic infection to malignant lymphoma. Host genetic factors significantly influence BLV susceptibility, proviral load (PVL), immune response, and disease progression. This mini-review synthesizes evidence on genetic polymorphisms in immune-related genes such as BoLA-DRB3, Tumor necrosis factor (TNF), and immunoglobulin loci, and examines novel findings from genome-wide association studies (GWAS). Beyond classical immune genes, recent GWAS have identified novel loci including SPATA16 (spermatogenesis associated 16), ABT1 (activator of basal transcription 1), IER3 (immediate early response 3), Adaptor Related Protein Complex 4 Subunit Beta 1 (AP4B1), Tripartite Motif Containing 45 (TRIM45), Patatin Like Phospholipase Domain Containing 1 (PNPLA1), and PRRC2A (proline-rich coiled-coil 2 A) that are implicated in transcriptional regulation, stress response, RNA processing, and intracellular transport, all of which may modulate viral replication and persistence. Understanding these genetic determinants provides new insights into host-virus interactions and offers opportunities for selective breeding strategies, biomarker development, and improved BLV control programs. - Source: PubMed
Publication date: 2025/11/17
Akbarin Mohammad MehdiFarjami ZahraÁlvarez Hugo Ramírez - The host defense system employs elaborate mechanisms to combat invading viruses. Here, we demonstrate that tripartite motif containing 45 (TRIM45) restricts the replication of different subtypes of influenza virus. TRIM45 interacted with and reduced the level of viral polymerase basic protein 2 (PB2). PB2 associated with heat shock cognate protein 70 (HSC70) and lysosomal-associated membrane protein type 2A (LAMP-2A), and was directed for lysosomal degradation via chaperone-mediated autophagy (CMA). TRIM45 promoted LAMP-2A expression and enhanced PB2/LAMP-2A binding, thereby facilitating CMA-dependent PB2 degradation. Mechanistically, TRIM45 employed its E3 ubiquitin ligase activity to mediate the K48-linked polyubiquitination and proteasomal degradation of Ca2 + -dependent cysteine protease calpain 1 (CAPN1), which prevented CAPN1-mediated cleavage of LAMP-2A. Sequence analysis identified a highly conserved QMRDV motif at position 602-606 of PB2, which was required for its binding with LAMP-2A or HSC70. Strikingly, mutations of this motif abolished this binding and the degradation effect of TRIM45 on PB2, and a PB2-Q602A mutant virus exhibited increased replication and enhanced pathogenicity in mice. Collectively, our findings reveal that TRIM45 restricts influenza virus infection by promoting the degradation of viral PB2 protein via CMA. - Source: PubMed
Publication date: 2025/10/23
Wang YihanJiang LiLi QibingLi MengyaShi WenjunWang BoWang GuangwenDeng GuohuaShi JianzhongTian GuobinZeng XianyingChen HualanLi Chengjun