Ask about this productRelated genes to: EXOSC2 antibody
- Gene:
- EXOSC2 NIH gene
- Name:
- exosome component 2
- Previous symbol:
- -
- Synonyms:
- hRrp4p, Rrp4p, RRP4, p7
- Chromosome:
- 9q34.12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-26
- Date modifiied:
- 2016-10-05
Related products to: EXOSC2 antibody
Related articles to: EXOSC2 antibody
- Protein kinases play a crucial role in regulating cellular processes, and their dysregulation is frequently implicated in various diseases, including cancer. Targeting protein kinases represents a promising therapeutic strategy for cancer treatment. Esophageal squamous cell carcinoma (ESCC) constitutes over 90% of esophageal cancer cases in high-incidence regions, with a global five-year survival rate below 20%. Here, we report that CK2 is aberrantly activated in ESCC, identified through kinase-substrate enrichment analysis (KSEA) of large-scale proteomic and phosphoproteomic data. Functional enrichment revealed the splicing factor SF3B3 as a clinically relevant CK2 substrate. We demonstrated that CK2-mediated phosphorylation of SF3B3 T1200 plays a pivotal role in ESCC progression. Mechanistically, CK2-mediated phosphorylation of SF3B3 enhances its affinity for the deubiquitinase USP7, leading to SF3B3 deubiquitination and subsequent protein stabilization. This stabilization drives ESCC progression by regulating alternative splicing (AS) events, including a critical event involving the inclusion of exon 4 in the EXOSC2 transcript. Furthermore, we demonstrated that SF3B3 T1200 phosphorylation specifically facilitates its incorporation into the U2 snRNP complex, directly promoting the aforementioned EXOSC2 exon 4 inclusion. Crucially, targeting CK2 or USP7, either individually or in combination, effectively suppressed ESCC progression. Our findings uncover a key molecular mechanism underlying SF3B3 stabilization and AS regulation, offering novel therapeutic opportunities for ESCC. - Source: PubMed
Publication date: 2026/04/10
Wang Du-ChuangLi Jia-YuanWang Xiao-BingHu Guo-ShengNie Rui-ChaoZheng BinHe Yao-HuiLiu Wen - Acute Myeloid Leukemia (AML) is an aggressive hematologic malignancy with significant clinical challenges due to its heterogeneity and high relapse rate. Dysregulated ribosome biogenesis is a recognized driver of tumorigenesis and therapy resistance, but its comprehensive impact on AML prognosis and the immune microenvironment remains to be fully elucidated. - Source: PubMed
Publication date: 2025/11/28
Chen XiaoheFeng AimeiChen FanZeng JueChen Ming - Focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) are major causes of primary nephrotic syndrome. However, the mechanisms of liquid-liquid phase separation (LLPS)-related genes in the development of FSGS and MCD remain unclear. We retrieved the Gene Expression Omnibus (GEO) database for the expression profiles of FSGS and MCD and identified the differentially expressed genes (DEGs) related to LLPS. Algorithms including Vector Machine-Recursive Feature Elimination (SVM-RFE) and Random Forest (RF) were adopted to identify the candidate genes. Functional enrichment analysis, nomogram, immune infiltration analysis, the receiver operating characteristic ROC) curve analysis, and external validation were performed. The research identified 59 and 40 DEGs related to LLPS for FSGS and MCD, respectively. Two candidate genes [PDS5 cohesin-associated factor A (PDS5A) and exosome component 2 (EXOSC2)] were obtained for FSGS, and three candidate genes [PDS5A, KH RNA-binding domain-containing signal transduction-associated 1 (KHDRBS1), and JunD proto-oncogene (JUND)] were obtained for MCD. Both the nomogram and ROC analysis indicated that the candidate genes had good predictive performance. For FSGS, the area under the curve (AUC) values of PDS5A and EXOSC2 were 0.994 and 0.806, respectively. For MCD, the AUC values of PDS5A, KHDRBS1, and JUND were 1, 0.896, and 0.958, respectively. Immune infiltration analysis revealed that FSGS patients had higher levels of naive B cells while MCD patients had higher levels of M2 macrophages and resting mast cells.PDS5A may represent a potential diagnostic biomarker, and targeting its aberrant phase separation may offer a therapeutic strategy for podocytopathies. - Source: PubMed
Publication date: 2025/10/19
Lu HuijuanSun JiaSun Jieqiong - Growth, fatness, and reproductive traits are key economic traits that significantly influence the efficiency and long-term sustainability of commercial pig production. While genome-wide association study (GWAS) has proven to be an effective approach for identifying genetic variants associated with key traits, the significant loci identified by GWAS do not necessarily correspond to the true causal genes. To address this, we performed GWAS on 4 560 pigs from three populations to investigate six traits: right teat number (RTN), left teat number (LTN), body length (BL), body height (BH), BW and backfat thickness (BFT). We incorporated three post-GWAS analyses: expression quantitative trait loci mapping, Bayesian colocalisation analysis, and Mendelian randomisation to prioritise candidate causal genes. Genes supported by at least two independent lines of evidence were prioritised as high-confidence causal candidates. GWAS identified one novel lead single nucleotide polymorphism (SNP) on Sus scrofa chromosome 7 (SSC7) for teat number and two new lead SNPs for BFT on SSC1 and SSC18. A total of 16 and 23 potential causal genes were identified for LTN and RTN, respectively. Among these, four genes (ABCD4, ALDH6A1, ENTPD5, and ISCA2) were supported by all four lines of evidence for both traits. For BL, four out of ten candidate genes (ABCD4, PTGR2, ENTPD5 and FAM161B) received full support. For BFT, two of 23 genes (EXOSC2 and USP20) were fully supported. Regarding BW, among six genes, ASS1 ranked the highest and was supported by three lines of evidence. For BH, 12 genes, including PTK6 and STMN3, were supported by two lines of evidence. In summary, the integration of GWAS with multiple post-GWAS analyses provides a powerful and systematic strategy to refine association signals and prioritise putative causal genes. The novel loci and candidate genes identified expand genetic resources for marker-assisted selection and provide insights into the genetic basis of growth performance and reproductive traits in the pig industry. - Source: PubMed
Publication date: 2025/09/09
Huang YWu FTang XLi JGe MWang MWei JXiao SZhang Z - Head and neck squamous cell carcinoma (HNSC) is a highly aggressive malignancy with poor prognosis, necessitating the identification of novel biomarkers for improved diagnosis and treatment. The exosome complex (EXOSC) family plays a crucial role in RNA metabolism, but its significance in HNSC remains poorly understood. We performed a comprehensive multi-omics analysis integrating data from TCGA, GEO, CPTAC, and the Human Protein Atlas to investigate the expression, prognostic value, and immune relevance of EXOSC genes in HNSC. We conducted differential expression analysis, survival analysis (OS, DSS, PFI), ROC curve evaluation, and clinicopathological correlation studies. Genetic alterations were examined using cBioPortal. Gene co-expression and enrichment analyses were used to elucidate potential molecular functions, and a protein-protein interaction (PPI) network was constructed via GeneMANIA. Immune infiltration, immune checkpoint correlations, and RNA modification associations were assessed using ssGSEA, Spearman correlation, and RNA modification databases. Experimental validation was performed by qRT-PCR in HNSC and normal cell lines. All EXOSC family members were significantly upregulated in HNSC tissues and cell lines. ROC analysis demonstrated favorable diagnostic potential, particularly for EXOSC2 (AUC = 0.910). Elevated expression of EXOSC2, EXOSC3, EXOSC8, and EXOSC9 was significantly associated with poor OS, DSS, and PFI. High expression of EXOSC2, EXOSC4, EXOSC5, and EXOSC9 correlated with advanced clinical stage, lymphovascular invasion, and poor therapeutic outcomes. cBioPortal analysis revealed EXOSC4 had the highest genetic alteration frequency (8%), primarily due to amplification. Immune infiltration analysis showed EXOSC gene expression was significantly correlated with various immune cell populations and immune checkpoint molecules, especially EXOSC3, EXOSC9, and EXOSC10. Functional enrichment and PPI network analyses indicated that EXOSC family genes participate in RNA metabolism, exoribonuclease activity, and immune-related pathways. A prognostic risk model based on EXOSC co-expressed genes demonstrated strong predictive performance for patient survival. Our study reveals that EXOSC family genes are significantly dysregulated in HNSC and are associated with tumor progression, prognosis, immune microenvironment modulation, and RNA modification. These findings highlight the potential of EXOSC members as novel diagnostic and prognostic biomarkers and suggest their relevance as therapeutic targets in HNSC. - Source: PubMed
Publication date: 2025/08/19
Zhang XuezhongZhao MengmengChu TingtingWei JiashaJia Qingmei