Ask about this productRelated genes to: ZNF709 Blocking Peptide
- Gene:
- ZNF709 NIH gene
- Name:
- zinc finger protein 709
- Previous symbol:
- -
- Synonyms:
- FLJ38281
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-04
- Date modifiied:
- 2014-11-19
Related products to: ZNF709 Blocking Peptide
Related articles to: ZNF709 Blocking Peptide
- Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease in which many patients respond inadequately to ursodeoxycholic acid (UDCA) and may progress to liver failure. Although research on PBC has primarily centered on lymphocyte-mediated mechanisms, increasing evidence implicates neutrophils in autoimmunity, yet their role in PBC remains unclear. - Source: PubMed
Publication date: 2026/07/08
Su MingxinTian ZhenfengYu MiaoHuang EnlaiLiang JinjianHu BingrongChen Yinting - Metastatic melanoma is an aggressive, heterogeneous cancer with early spread and poor prognosis. Transcriptomic analysis identifies potential therapeutic targets. In silico analysis of the GEO dataset GSE7553 compared primary vs metastatic melanoma using differential expression, enrichment (GO/KEGG/Reactome), PPI network construction, and hub-gene prioritization. Candidates were validated through survival analysis, mutation-associated analyses, and virtual screening using molecular docking with FDA-approved compounds. Transcriptomic results show divergence between primary and metastatic melanoma samples, with principal component analysis supporting clear group separation. In a total of 54,675 probe-level entries, 4868 were classified as upregulated and 10,269 as downregulated, indicating a predominance of downregulated transcriptional events in metastatic melanoma. Prioritized upregulated genes included CUL5, ZC3H14, SON, BRCC3, and H3-3B, whereas notable downregulated genes included ZNF709, CD84, STARD8, EPOR, and HAVCR2. The high-confidence PPI network comprised 625 nodes and 2661 edges, with a significant enrichment score. Enrichment analysis implicated immune/adhesion and translation pathways (e.g., Rap1, focal adhesion, T-cell activation). Survival: CUL5 (HR = 0.26) and ZC3H14 (HR = 0.60) are protective, while SON (HR = 2.4) is adverse. Mutation-linked transcriptomic analysis identified 10 significantly altered genes, including downregulated SNHG18 and upregulated LPCAT2. Virtual screening results show repurposable compounds, with Floxacrine showing strong predicted affinity for CUL5 and Dihydroergocristine showing favorable interaction with LPCAT2/ZC3H14-related targets. In silico docking results further supported CUL5-Floxacrine and LPCAT2-Dihydroergocristine as notable candidate interactions. Results show key transcriptomic drivers and targets (CUL5, ZC3H14, SON, BRCC3, LPCAT2) in metastatic melanoma. Results highlight a useful hypothesis-generating framework for biomarker prioritization and drug repurposing in melanoma. However, independent cohort validation and experimental confirmation are required before clinical translation. - Source: PubMed
Publication date: 2026/05/02
Majeed Khulood AyadMajeed Raghad AyadIbrahim Taisir KhalilKhan Najeeb Ullah - Poly(C)-binding protein 4 (PCBP4), also called MCG10 and a target of p53, plays a role in the cell cycle and is implicated in lung tumor suppression. Here, we found that PCBP4-deficient mice are prone to lung adenocarcinoma, lymphoma, and kidney tumor and that PCBP4-deficient mouse embryo fibroblasts (MEFs) exhibit enhanced cell proliferation but decreased cellular senescence. We also found that p53 expression is markedly reduced in PCBP4-deficient MEFs and mouse tissues, suggesting that PCBP4 in turn regulates p53 expression. To determine how PCBP4 regulates p53 expression, PCBP4 targets were identified by RNA immunoprecipitation followed by RNA sequencing (RNA-seq). We found that the transcript encoding ZFP871 (zinc finger protein 871; also called ZNF709 in humans) interacts with and is regulated by PCBP4 via mRNA stability. Additionally, we found that ZFP871 physically interacts with p53 and MDM2 proteins. Consistently, ectopic expression of ZFP871 decreases-whereas knockdown of ZFP871 increases-p53 protein stability through a proteasome-dependent degradation pathway. Moreover, loss of ZFP871 reverses the reduction of p53 expression by lack of PCBP4, and thus increased expression of ZFP871 is responsible for decreased expression of p53 in the PCBP4-deficient MEFs and mouse tissues. Interestingly, we found that, like PCBP4, ZFP871 is also regulated by DNA damage and p53. Finally, we showed that knockdown of ZFP871 markedly enhances p53 expression, leading to growth suppression and apoptosis in a p53-dependent manner. Thus, the p53-PCBP4-ZFP871 axis represents a novel feedback loop in the p53 pathway. Together, we hypothesize that PCBP4 is a potential tissue-specific tumor suppressor and that ZFP871 is part of MDM2 and possibly other ubiquitin E3 ligases that target p53 for degradation. - Source: PubMed
Publication date: 2016/02/25
Yan WenshengScoumanne ArianeJung Yong-SamXu EnshunZhang JinZhang YanhongRen CongSun PeiChen Xinbin