Ask about this productRelated genes to: ZNF117 antibody
- Gene:
- ZNF117 NIH gene
- Name:
- zinc finger protein 117
- Previous symbol:
- -
- Synonyms:
- HPF9, H-plk
- Chromosome:
- 7q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-05-19
- Date modifiied:
- 2016-10-05
Related products to: ZNF117 antibody
Related articles to: ZNF117 antibody
- BACKGROUND: Obstructive sleep apnea (OSA) and sarcopenia are common age-related conditions that significantly reduce quality of life. OSA is characterized by recurrent breathing interruptions and chronic intermittent hypoxia, while sarcopenia involves progressive loss of muscle mass and strength. Accumulating evidence indicates that chronic intermittent hypoxia and sleep fragmentation in OSA may promote muscle wasting via inflammatory pathways (e.g., NF-κB), oxidative stress, and impaired protein synthesis. Conversely, sarcopenia-related muscle weakness may worsen upper airway collapsibility, creating a vicious cycle. However, the molecular mechanisms linking OSA and sarcopenia remain poorly understood. METHODS: We performed differential expression analysis on OSA and sarcopenia datasets from the Gene Expression Omnibus (GEO) and used weighted gene co-expression network analysis (WGCNA) to identify candidate biomarkers, with functional enrichment assessed under false discovery rate (FDR) correction. A diagnostic model was constructed based on key genes and validated using receiver operating characteristic (ROC), calibration, and decision curves. Immune cell infiltration was analyzed using the CIBERSORT algorithm. RESULTS: We identified 123 differentially expressed genes shared by OSA and sarcopenia, enriched in pathways related to muscle function, cellular stress, metabolic disorders, and neurodegeneration. WGCNA identified ESF1, ZNF117, and C2orf49 as core genes. The diagnostic model showed high accuracy (area under the curve (AUC): 0.912 for OSA, and 0.967 for sarcopenia in training; 0.787 for OSA, and 0.744 for sarcopenia in validation). These genes were closely associated with pro-inflammatory immune cells. CONCLUSION: This study identifies ESF1, ZNF117, and C2orf49 as potential shared biomarkers for OSA and sarcopenia. The robust diagnostic model and the observed tissue-specific gene dysregulation illuminate the systemic interplay between these conditions, offering insights for risk stratification and future mechanistic research. - Source: PubMed
Publication date: 2026/03/05
Jiang FeiXu YangZheng BinZhang Guang-LeiLi Ren-Hu - The epigenome may represent a link between environmental factors and the genome in determining obesity risk. Alterations in the methylation pattern in DNA can affect gene expression. Therefore, the objective of this study was to evaluate global DNA methylation in children who develop obesity, establishing a comparison between them according to birth weight. - Source: PubMed
Publication date: 2025/09/16
Alfaro Juan ManuelVasquez Elsa MaríaRodriguez-Osorio NélidaUrrego Rodrigo - Traditional paradigms of pharmaceutical innovation have long relied on the "one drug, one disease" premise. However, a network mindset in unpacking disease mechanisms can be fruitful to move toward a "one drug, polydisease" paradigm of drug discovery and development. A case in point is obstructive sleep apnea (OSA) and lung cancer, which are two prevalent respiratory disorders that share common risk factors and may potentially exhibit overlapping molecular mechanisms. The putative mechanistic linkages between OSA and lung cancer remain underexplored; however, this study offers new evidence on overlapping genetic signatures between OSA and lung cancer with an in-silico approach. Bioinformatics analysis of the publicly available datasets (GSE135917 and GSE268175) identified 123 upregulated and 13 downregulated genes in OSA and 3175 upregulated and 2272 downregulated genes in lung cancer. A total of four genes (, , , and ) were significantly upregulated with both disorders, highlighting potentially shared genetic and molecular mechanisms. Pathway and cell enrichment analysis indicated that mucin type O-glycan biosynthesis pathway and endothelial cells are strongly associated with these shared genes, lending support for their potential roles in both diseases. Moreover, hsa-miR-34a-5p, hsa-let-7g-5p, and hsa-miR-19a-3p were found to be associated with these common genes. Validation using the GEPIA2 tool confirmed the consistent expression patterns of these four genes in lung cancer. Machine learning analysis highlighted as the most significant biomarker candidate for distinguishing OSA and lung cancer from controls. In summary, this study supports the overarching concept that human diseases can have shared mechanistic pathways in the specific example of OSA and lung cancer. While these findings call for further research and validation, they invite rethinking the current pharmaceutical innovation paradigms to move beyond the "one drug, one disease" concept. - Source: PubMed
Publication date: 2025/04/08
Dasgupta Sanjukta - Rare coding alleles play crucial roles in the molecular diagnosis of genetic diseases. However, the systemic identification of these alleles has been challenging due to their scarcity in the general population. Here, we discovered and characterized rare coding alleles contributing to genetic dyslipidemia, a principal risk for coronary artery disease, among over a million individuals combining three large contemporary genetic datasets (the Million Veteran Program, n = 634,535, UK Biobank, n = 431,178, and the All of Us Research Program, n = 92,304) totaling 1,158,017 multi-ancestral individuals. Unlike previous rare variant studies in lipids, this study included 238,243 individuals (20.6%) from non-European-like populations. Testing 2,997,401 rare coding variants from diverse backgrounds, we identified 800 exome-wide significant associations across 209 genes including 176 predicted loss of function and 624 missense variants. Among these exome-wide associations, 130 associations were driven by non-European-like populations. Associated alleles are highly enriched in functional variant classes, showed significant additive and recessive associations, exhibited similar effects across populations, and resolved pathogenicity for variants enriched in African or South-Asian populations. Furthermore, we identified 5 lipid-related genes associated with coronary artery disease . Among them, is a potentially novel therapeutic target through the down regulation of LDLC by its silencing. This study provides resources and insights for understanding causal mechanisms, quantifying the expressivity of rare coding alleles, and identifying novel drug targets across diverse populations. - Source: PubMed
Publication date: 2024/09/18
Koyama SatoshiYu ZhiChoi Seung HoanJurgens Sean JSelvaraj Margaret SunithaKlarin DerekHuffman Jennifer EClarke Shoa LTrinh Michael NRavi AkshayaDron Jacqueline SSpinks CatherineSurakka IdaBhatnagar AarushiLannery KimHornsby WhitneyDamrauer Scott MChang Kyong-MiLynch Julie AAssimes Themistocles LTsao Philip SRader Daniel JCho KellyPeloso Gina MEllinor Patrick TSun Yan VWilson Peter WfProgram Million VeteranNatarajan Pradeep - The identification of reliable prognostic markers is crucial for optimizing patient management and improving clinical outcomes in clear cell renal cell carcinoma (ccRCC). - Source: PubMed
Publication date: 2024/07/18
Yang Dongsheng