Ask about this productRelated genes to: NUP210 antibody
- Gene:
- NUP210 NIH gene
- Name:
- nucleoporin 210
- Previous symbol:
- -
- Synonyms:
- GP210, POM210, FLJ22389, KIAA0906
- Chromosome:
- 3p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-17
- Date modifiied:
- 2016-10-05
Related products to: NUP210 antibody
Related articles to: NUP210 antibody
- To explore the impact and establish biochemical response criteria for optimized risk stratification for anti-glycoprotein (gp) 210 and anti-centromeric antibodies (ACA) dual positivity on the prognosis of patients with primary biliary cholangitis (PBC). A retrospective cohort study was conducted, including 1 286 PBC patients who visited the Department of Gastroenterology, First Affiliated Hospital of Air Force Medical University, from June 2006 to March 2025. Patients were grouped according to their serum autoantibody status. Clinical data such as baseline demographic characteristics, laboratory indicators, and histological staging were collected. The endpoint events were complications of cirrhosis (ascites, hepatic encephalopathy, variceal bleeding, etc.), hepatocellular carcinoma, liver transplantation, or death. Statistical analysis was performed using SPSS 26.0 software. Survival curves were plotted using the Kaplan-Meier method. The log-rank test was used to compare differences between groups. ROC curves were plotted to compare the predictive performance of different biochemical response criteria. Continuous data were compared using the independent samples -test or the Mann-Whitney rank-sum test between the groups. Categorical data were compared using the test or Fisher's exact test between the groups. Patients with dual positivity for anti-gp210 antibody and ACA had significantly shorter event-free survival (<0.05). Early-stage patients with dual positivity had a significantly higher incidence of adverse events than other groups (46.05%, <0.05), along with lower serum albumin (ALB) and platelet count (PLT) levels (<0.05). The area under the curve (AUC) was 0.873 (95%: 0.771-0.975) for the biochemical response criteria based on ALB ≥1×lower limit of normal (LLN) and PLT ≥1×LLN after one year of ursodeoxycholic acid (UDCA) treatment. The incidence rate of adverse events in biochemical respondents was 4.3%, which was superior to other biochemical response criteria in predicting adverse events in early-stage dual-positive patients (<0.05). However, there was no statistically significant difference in the incidence of endpoint events among the different biochemical response criteria groups in late dual-positive patients (>0.05). PBC patients with dual positivity for anti-gp210 antibody and ACA have a poorer prognosis and exhibit a high risk of decompensation in the early stages of disease. Biochemical response criteria based on ALB and PLT can accurately identify high-risk patients with dual positivity at an early stage, providing an objective basis for implementing early intensive intervention strategies for high-risk patients in clinical practice. - Source: PubMed
Luo JDing D WGuo G YSu S HYang C YJia GSun R QDeng JZheng L HLuo G HYin FLiu Y SCui L NGuo C CZhou X MShang Y LHan Y - Prostate cancer (PCa) is an age-related epithelial malignancy with high metastatic potential. Although nucleoporin 210 (NUP210) is implicated in tumor progression, its role and mechanism in PCa metastasis remain unexplored. - Source: PubMed
Publication date: 2026/02/23
Wang ShaoxingLi JinmingJiang JunLiu JiahaoZuo Shusen - Hepatocellular carcinoma (HCC) remains a highly lethal malignancy despite therapeutic advances. SMARCB1 exhibits context-dependent functions across different cancer types. While it is frequently inactivated as a tumor suppressor in various malignancies, our previous work demonstrated that SMARCB1 acts as an oncogene in HCC by engaging the NUP210-P300 transcriptional axis. However, the upstream mechanisms that regulate SMARCB1 stability in HCC remain unexplored. Because SMARCB1 undergoes ubiquitin-mediated degradation under hypoxic conditions in other contexts, we investigated whether this regulation occurs in HCC. Cycloheximide (CHX) chase assays revealed that SMARCB1 remained highly stable under hypoxia in HCC cells, suggesting the presence of an active stabilization mechanism. Our screening for post-translational regulators identified USP21 as a deubiquitinase modulating SMARCB1 turnover. TCGA-LIHC analysis showed that USP21 is upregulated in HCC and positively correlated with SMARCB1 expression. Loss- and gain-of-function experiments confirmed that USP21 inhibition promotes SMARCB1 degradation, while USP21 overexpression prevents it. Co-immunoprecipitation demonstrated a physical interaction between USP21 and SMARCB1 that blocks ubiquitin-mediated proteasomal degradation. Combined inhibition of USP21 and P300, a downstream effector of SMARCB1, more effectively suppressed HCC cell proliferation under hypoxia than either treatment alone. Transcriptomic analysis further revealed that USP21-SMARCB1 axis contributes to immune-tolerant features in HCC. USP21 stabilizes SMARCB1 under hypoxic conditions, thereby sustaining its oncogenic and immunosuppressive activities in HCC. Targeting the USP21-SMARCB1 axis may inhibit tumor growth and enhance immunotherapy responsiveness, offering a potential therapeutic strategy for overcoming resistance in HCC treatment. - Source: PubMed
Publication date: 2026/01/30
Kim MinhoKim Myoung JunChoi Sung KyungYu BitnuriChoi Un YungHwang SunsookChoi Wahn SooYou Jueng Soo - A highly curved membrane region connecting the inner and the outer nuclear membrane serves as a platform where nucleoporins with one or more transmembrane domains promote anchoring of the nuclear pore complex to the nuclear envelope. In mammalian cells, three transmembrane nucleoporins, Nup210, POM121 and NDC1, are inserted at this site. Here, we characterize TMEM209, which had initially been identified as a protein concentrated at the nuclear envelope, as a fourth transmembrane nucleoporin. Proximity labeling revealed that TMEM209 is present close to proteins of the inner nuclear membrane and to other nucleoporins. TMEM209 localized to the nuclear pore complex in immunofluorescence microscopy and biochemically interacted with Nup210 via a region containing its two transmembrane domains. TMEM209 depletion impaired cell growth and delayed entry into S, G2 and M phases of the cell cycle. Conversely, its overexpression specifically dissociated Nup210 from the nuclear envelope. Together, these findings establish TMEM209 as a novel transmembrane nucleoporin that cooperates with Nup210 in cell cycle progression and cell proliferation. - Source: PubMed
Publication date: 2026/02/24
Kohlhause DavidSpillner ChristianeAlcalde Zapata VioletaLenz ChristofUrlaub HenningKohl TobiasLehnart Stephan EGerace LarryKehlenbach Ralph H - Hypertrophic cardiomyopathy (HCM) is a prevalent cardiovascular disorder affecting populations worldwide, characterized by abnormal thickening of the heart muscle.(Supporting S1) The development of HCM is influenced by multiple factors, including genetic mutations, geographical conditions, lifestyle, and environmental exposures. The availability of extensive genomic datasets in public repositories provides an opportunity to identify potential genetic contributors and functional biomarkers associated with HCM. Previous studies have highlighted the pivotal role of the MYBPC3 gene in the pathogenesis of HCM. In this study, computational analyses were performed to predict gene mutations and functional biomarkers using RNA-sequencing and whole exome sequencing datasets. A total of 12 RNA-sequencing samples, comprising four healthy controls and eight HCM cases, along with 12 exome sequencing datasets, were retrieved from the Gene Expression Omnibus (GEO) database. RNA-sequencing analysis identified the top 20 differentially expressed genes associated with HCM, including MIB2, ZBTB48, MYBPC3, PRPF40B, CD27-AS1, MYH7, WDR90, KDM8, BCAM, ZSWIM9, KANK3, CCDC85A, ZNF512B, POLR3H, NUP210, PSMG4, GPLD1, GNL1, SH2D3C, and COL4A6. Among these, MYH7 exhibited the highest expression level, showing strong similarity to MYBPC3 in its association with HCM. Whole exome sequencing analysis further identified a panel of variant genes including MYBPC3, MYH6, MYH7, TNT, Titin, Desmin, ACE1, TGF-beta, Ang-2, SGCG, SGCA, DMD, and LaminA/C, all previously implicated in HCM pathophysiology. This integrative study underscores the correlation between differential gene expression patterns and clinical variants in HCM, providing valuable insights into the molecular mechanisms underlying the disease. - Source: PubMed
Publication date: 2025/11/21
Cn PrashanthaR RamachandraNm GuruprasadReddy Vaddi Damodara