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
- 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 - Fetal growth restriction (FGR) is a significant contributor to negative pregnancy and postnatal developmental outcomes. Currently, the exact pathological mechanism of FGR remains unknown. This study aims to utilize multiomics sequencing technology to investigate potential relationships among mRNA, gut microbiota, and metabolism in order to establish a theoretical foundation for diagnosing and understanding the molecular mechanisms underlying FGR. - Source: PubMed
Publication date: 2024/04/05
Tang HuiLi DanPeng JingYang WeitaoZhang XianLi Hanmei - Hepatocellular carcinoma (HCC) is a prevalent malignancy characterized by complex heterogeneity and drug resistance. Resistance to ferroptosis is closely related to the progression of HCC. While HCC tumors vary in their sensitivity to ferroptosis, the precise factors underlying this heterogeneity remain unclear. In this study, we sought to elucidate the mechanisms that contribute to ferroptosis resistance in HCC. Whole-genome CRISPR/Cas9 screen using a subtoxic concentration (IC20) of ferroptosis inducer erastin in the HCC cell line Huh7 revealed TRIM34 as a critical driver of ferroptosis resistance in HCC. Further investigation revealed that TRIM34 suppresses ferroptosis in HCC cells, promoting their proliferation, migration, and invasion both in vitro and in vivo. Furthermore, TRIM34 expression is elevated in HCC tumor tissues, correlating with a poor prognosis. Mechanistically, TRIM34 directly interacts with Up-frameshift 1 (UPF1), a core component of the nonsense-mediated mRNA decay (NMD) pathway, to promote its ubiquitination and degradation. This interaction suppresses GPX4 transcript degradation, thus promoting the protein levels of this critical ferroptosis suppressor in HCC. In light of the close crosstalk between ferroptosis and the adaptive immune response in cancer, HCC cells with targeting knockdown of TRIM34 exhibited an improved response to anti-PD-1 treatment. Taken together, the TRIM34/UPF1/GPX4 axis mediates ferroptosis resistance in HCC, thereby promoting malignant phenotypes. Targeting TRIM34 may thus represent a promising new strategy for HCC treatment. - Source: PubMed
Publication date: 2024/05/03
Yao FeifanZhou SuiqingZhang RuizhiChen YiningHuang WeiYu KaiYang NanmuQian XiangjunTie XiaofengXu JialiZhang YuBaheti TasikenXu JingDai XinzhengHao XiaopeiZhang LirenWang XuehaoLi Qing