Ask about this productRelated genes to: TRIM34 antibody
- Gene:
- TRIM34 NIH gene
- Name:
- tripartite motif containing 34
- Previous symbol:
- RNF21
- Synonyms:
- -
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2016-11-10
Related products to: TRIM34 antibody
Related articles to: TRIM34 antibody
- Primary ciliary dyskinesia (PCD) is a genetically heterogeneous disorder, and despite advances in next-generation sequencing, a substantial proportion of clinically suspected pediatric cases remain without a molecular diagnosis. This persistent diagnostic gap reflects limitations of earlier analysis pipelines and incomplete knowledge of PCD-related genes. Reanalysis of existing whole-exome sequencing (WES) data using updated resources has become a practical strategy to improve diagnostic yield in pediatric populations. - Source: PubMed
Hakçıl Öz TilbeŞişmanlar Eyüboğlu TuğbaAslan Ayşe TanaKula NilgünKayhan Gülsüm - The tripartite motif-containing (TRIM) 34 protein is an interferon (IFN)-induced protein whose expression is upregulated after influenza A virus (IAV) infection. Here, we identify a previously unknown function for TRIM34 as a negative regulator of innate immune responses following IFN treatment and IAV infection, even in mice, suggesting that this effect is broad and conserved. Complementary overexpression and silencing experiments in cultured cells show that TRIM34 expression positively correlates with IAV titers, indicating that TRIM34 promotes viral replication, likely by counteracting antiviral responses. Moreover, we show novel interactions of TRIM34 with cellular proteins involved in the nucleocytoplasmic transport of host mRNAs and proteins, even in mock-infected cells. Remarkably, these TRIM34 interactions seem independent of TRIM34 E3 ubiquitin ligase activity and affect the nuclear import of IFN-regulatory factor 3 (IRF3) and the nuclear export of host mRNAs encoding antiviral functions, without affecting the nuclear export of viral mRNAs. These results provide a likely mechanism by which TRIM34 dampens host innate immune responses. These TRIM34-mediated effects could be further exploited to develop new antiviral drugs against IAV, and potentially other viral infections. - Source: PubMed
Publication date: 2026/05/20
Vázquez-Utrilla PaulaRivero VanessaDeDiego Marta L - Idiopathic interstitial pulmonary fibrosis (IPF) is a chronic and progressive disease characterized by interstitial fibrosis, with poor prognosis and high mortality. TRIM34 is involved in the intracellular ubiquitination process, but its mechanism of action in IPF is currently unknown. The purpose of this study was to investigate the effect of TRIM34 on the IPF process and its mechanism. In this study, 5 mg/kg of bleomycin (BLM) was injected into the rat trachea to construct the IPF animal model, and 10 ng/mL of VEGF165 was added to human pulmonary microvascular endothelial cell (HPMECs) culture medium to construct the angiogenic cell model. The expression of proteins was detected by Western blot. The assessment of proliferation, angiogenesis, and fibrosis in HPMECs and rat lung tissue was conducted using EdU staining, scratch tests, angiogenesis tests, HE staining, and Masson staining. The research indicated a reduction in TRIM34 expression in IPF. Overexpression of TRIM34 significantly improved pulmonary inflammatory infiltration in IPF rats, restored alveolar structure, reduced collagen deposition in lung tissue, upregulated the expression of E-cadherin, downregulated the expression of COL-I, COL-III, a-SMA, CD31, CD34, and VEGFA, and finally alleviated the progression of IPF in rats. In addition, overexpression of TRIM34 also inhibited VEGF-induced proliferation, migration, and angiogenesis of HPMECs by inhibiting glucose uptake and pyruvate, lactic acid, and ATP content of HPMECs. In terms of mechanism, Tianlongjie (TL) therapy promotes HIF-1A ubiquitination degradation by upregulating TRIM34 expression, thereby inhibiting glycolysis, reducing angiogenesis, and alleviating IPF progression. In conclusion, TL therapy inhibits angiogenesis by upregulating TRIM34 expression and ultimately alleviates IPF progression. - Source: PubMed
Yang ChunyanLiu QingChen BingJing HaiqingWang YanqiongChen BinSong JiayiFu Yi - TRIM34, an E3 ubiquitin ligase, plays a pivotal role in regulating protein degradation, the cell cycle, and tumor progression. So far, the precise mechanisms and function of TRIM34 in triple-negative breast cancer (TNBC) remain unclear. In this study, we investigated the effect of TRIM34 in TNBC through in vitro and in vivo experiments. We identified TRIM34 as a significant regulator of Fatty Acid Synthase (FASN). TRIM34 was found to be downregulated in TNBC tissues, and its overexpression inhibited cell proliferation and migration by reducing fatty acid synthesis. Mechanistically, TRIM34 directly interacts with FASN, promoting its K48-linked ubiquitination and degradation. Clinical analysis revealed a negative correlation between TRIM34 and FASN expression, and low TRIM34 levels associated with poor patient prognosis. TRIM34 is a tumor suppressor and impedes TNBC progression by targeting FASN, offering a promising avenue for therapeutic intervention. - Source: PubMed
Publication date: 2025/06/19
Li YongShan JijunLiu ShanqingShen YanNiu LianjieMao QixinChen Xiaobing - Despite breakthroughs in our understanding of lung cancer risk, development, immunologic control, and therapy choices, it remains one of the leading causes of cancer mortality. This study aimed to investigate the role of TRIM34 upon treatment of Interferon Gamma (IFN-γ) in Non-Small Cell Lung Cancer (NSCLC). NCI-H23 cells were exposed to IFN-γ in a dose- and time-dependent manner to understand TRIM34 expression and its role as a co-regulator of treatment. The regulatory role of TRIM34 on IFN-γ exposure was studied by qRT-PCR, Western blot analysis, immunocytochemistry, apoptosis assay and scratch assay. On exposure to IFN-γ, TRIM34 expression at transcript and protein level was significantly upregulated. With its upregulation, NCI-H23 underwent apoptosis and its rate of proliferation was impeded. Our results suggest that induction of TRIM34 by IFN-γ treatment may lead to an anti-tumor inflammatory response, resulting in NSCLC regression via apoptosis. - Source: PubMed
Chaudhari KaushalkumarVasu Vihas TGolani AparnaShaikh AfridiNagariya NidhiRoy Hetal