Ask about this productRelated genes to: USP34 antibody
- Gene:
- USP34 NIH gene
- Name:
- ubiquitin specific peptidase 34
- Previous symbol:
- -
- Synonyms:
- KIAA0570, KIAA0729
- Chromosome:
- 2p15
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-04
- Date modifiied:
- 2016-10-05
Related products to: USP34 antibody
Related articles to: USP34 antibody
- Triple-negative breast cancer (TNBC) represents a particularly aggressive form of breast tumors. Mitochondrial dysfunction represses the proliferation of TNBC cells. Ubiquitin-specific proteases 34 (USP34) has been predicted to be abnormally overexpressed in TNBC. This research examined the role of USP34 in the mitochondrial function modulation of TNBC. Herein, cell proliferation was evaluated by the 5-ethynyl-2'-deoxyuridine assay. Mitochondrial membrane potential was detected employing the JC-1 assay. Mitochondrial superoxide was measured utilizing MitoSOX Red assay. Mito‑Tracker Red CMXRos staining was selected to monitor mitochondrial network structure. The relationship among USP34, eukaryotic translation initiation factor 3 m (eIF3m), and mitochondrial carrier homolog 2 (MTCH2) was validated by co-immunoprecipitation, GST-pull down, RNA immunoprecipitation and RNA-pull down analysis. We found that USP34 silencing inhibited cell proliferation by inducing mitochondrial dysfunction in TNBC cells. USP34 maintained the stability of the eIF3m protein through deubiquitination. Overexpression of eIF3m countered the mitochondrial dysfunction induced by USP34 silencing. Furthermore, eIF3m upregulated the MTCH2 level by directly binding to its 5'UTR region. MTCH2 overexpression reversed the damaging effect of eIF3m silencing on mitochondrial function. Collectively, USP34 maintained the stability of eIF3m protein through deubiquitination; the upregulated eIF3m bound to the 5'UTR of MTCH2 mRNA to promote MTCH2 expression, thereby maintaining mitochondrial function and promoting the malignant progression of TNBC. - Source: PubMed
Publication date: 2026/04/23
Qian Peng-FeiZeng YiZhong Wang-Jing - Identifying patients most likely to benefit from immune checkpoint inhibitors (ICIs) remains a significant challenge in advanced melanoma. We evaluated the association between tumor somatic mutations and clinical outcomes, focusing on relapse-free survival (RFS) and overall survival (OS) in locoregionally advanced melanoma patients treated with neoadjuvant ipilimumab. Tumor specimens and matched peripheral blood samples from 22 patients underwent whole-exome sequencing (WES) to identify non-synonymous somatic mutations. Tumor mutational burden (TMB) was quantified, and specific mutations were analyzed for associations with survival outcomes. The analysis revealed a mutational landscape dominated by single-nucleotide missense mutations with a median TMB of 11.4 mutations/MB. and mutations were detected in 73% of patients and exhibited mutual exclusivity and concurrence patterns ( < 0.05). Positional clustering identified and as key contributors to melanoma (FDR -value < 0.05). Log-rank analysis indicated that mutations in , , , , , , and were associated with shorter survival outcomes (RFS or OS). The associations remained significant in both univariate and multivariable Cox regression models adjusted for TMB. These genes can be broadly grouped into functional categories relevant to tumor progression and immune modulation. In applying multiple testing correction, none maintained statistical significance, indicating that these findings should be interpreted as exploratory and require validation in independent cohorts. This study identified tumor genomic alterations associated with clinical outcomes in melanoma patients treated with neoadjuvant ipilimumab, suggesting their potential role in anti-tumor immunity. These findings warrant further investigation in larger cohorts and across other ICIs in melanoma and other malignancies. - Source: PubMed
Publication date: 2026/03/19
Khaksar Mohammad AliEljilany IslamYassine IbrahimYu XiaoqingTeer Jamie KConejo-Garcia Jose RLyons MaureenLaFramboise WilliamTarhini Ahmad A - Recent advances in genomic technologies have greatly enhanced our understanding of genotype-phenotype relationships and improved the diagnosis of genetic diseases. However, the dissection of complex structural variants (SVs) remains challenging due to the limitations of current methods in resolving their breakpoints and interpreting phenotypes involving multiple disrupted genes. In this study, we demonstrate how an integrative approach-combining molecular cytogenetic, genomic, and transcriptomic methods-enables the detection and structural and functional characterization of complex SVs affecting the MBD5, USP34, and XPO1 genes. Our findings underscore the utility of the Exo-C, a modified chromosome conformation capture technique in resolving complex rearrangements. We also report, for the first time, a composite neurodevelopmental phenotype resulting from the combined effects of MBD5-associated intellectual disability and 2p15p16.1 microdeletion syndromes. - Source: PubMed
Gridina MariaLagunov TimofeyBelokopytova PolinaTorgunakov NikitaNurislamov ArtemYurchenko Darya AMarkova Zhanna GMarkova Tatiana VStepanchuk YanaKoksharova GalinaOrlov PavelSubbotovskaia AnnaRyzhkova OxanaShilova Nadezhda VFishman Veniamin - The pain and dysfunction caused by temporomandibular joint osteoarthritis (TMJ OA) can be debilitating. However, effective disease-modifying medicine for TMJ OA remains an unfulfilled need. While progressive cartilage degradation represents the hallmark of TMJ OA, the underlying molecular mechanisms remain incompletely understood. Here, we identify ubiquitin-specific protease 34 (USP34) as a key regulator of mitochondrial quality control in TMJ chondrocytes through its stabilization of adenine nucleotide translocase 1 (ANT1). Using chondrocyte-specific KO ( ) mice, we first demonstrated age-dependent TMJ OA development characterized by cartilage destruction. Subsequent unilateral bite-raising experiments revealed that USP34 deficiency exacerbated mechanical stress-induced TMJ degeneration. Our results disclosed the dual protective role of USP34 against both age-related and mechanical stress-related TMJ degeneration. Mechanistically, we define the USP34-ANT1 axis as a component upstream of the PINK1-Parkin pathway. USP34 deubiquitinates and stabilizes ANT1, thereby promoting the initiation of Parkin-dependent mitophagy. Additionally, USP34 overexpression confers protection to chondrocytes against cellular injury. These findings establish USP34 as a critical node linking ubiquitin signaling to mitochondrial homeostasis in TMJ chondrocytes and propose targeting USP34 or ANT1 as a potential disease-modifying strategy. - Source: PubMed
Publication date: 2026/01/12
Jiang ShuangChen DanlingSheng RuiYuan QuanPan JianGuo Yuchen - Gastric cancer (GC) continues to be a fatal disease globally, largely due to the lack of dependable molecular indicators enabling early diagnosis and therapeutic intervention. Single-cell transcriptomic analysis revealed significant enrichment of DAZAP1 in proliferating and malignant gastric epithelial cells. Using a combined analysis of single-cell and bulk RNA-seq datasets, we further recognized DAZAP1 as a putative oncogene correlated with poor clinical outcomes in GC. Functional experiments demonstrated that DAZAP1 promotes tumor proliferation, cell cycle progression, and chemotherapy resistance in vitro and in vivo. Mechanistically, DAZAP1 bound and stabilized USP34 mRNA, leading to increased USP34 protein expression, which in turn mediated the deubiquitination and stabilization of the oncoprotein PIN1. This subsequently resulted in activation of the MAPK signaling pathway, driving GC progression and chemoresistance. Furthermore, we revealed that DAZAP1 expression is post-transcriptionally regulated by m6A modification through the demethylase ALKBH5, which protects DAZAP1 mRNA from YTHDF2-mediated degradation. Collectively, our findings establish the ALKBH5/DAZAP1/USP34/PIN1/MAPK axis as a key regulatory mechanism in gastric tumorigenesis and chemoresistance, underscoring DAZAP1 as a promising candidate for therapeutic and diagnostic applications in GC. - Source: PubMed
Publication date: 2025/12/02
Zhang PeilingMa LujuanWei YitianPeng QianXiang HongFang XishengWeng ChengyinWu YongLu Lin