Ask about this productRelated genes to: ZNF501 Blocking Peptide
- Gene:
- ZNF501 NIH gene
- Name:
- zinc finger protein 501
- Previous symbol:
- ZNF52
- Synonyms:
- MGC21738
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-03
- Date modifiied:
- 2016-10-05
Related products to: ZNF501 Blocking Peptide
Related articles to: ZNF501 Blocking Peptide
- The bighorn sheep (), despite its close relation to domestic sheep, suffer higher morbidity and mortality from respiratory disease complexes, likely due to genetic differences in immune responses. Unraveling highly repetitive regions such as immune loci and genetic differences was problematic until now. We generated a bighorn sheep telomere-to-telomere assembly, adding 14.28% of novel sequence compared to the previous reference. This enabled the first complete immune loci annotation revealing the IGL and TR loci are significantly short in bighorn sheep. Importantly, a critical immune gene and , involved in Golgi-mediated immune response, are lacking in bighorn but present in domestic sheep. Re-analysis of a carriage study, using this assembly, identified the immune gene as a key genetic marker for disease carriage, not observable in the original study. This work provides a critical resource for identifying phenotype-linked genetic variation and exploring evolutionary adaptations of bighorn sheep. - Source: PubMed
Publication date: 2025/10/02
Olagunju Temitayo APospelova MariiaSchwartz John CMousel Michelle RPiel Lindsay M WGrossman Paige CHuyvaert Kathryn PKuhn Kristen LRaihan TajbirStegemiller Morgan RKhilji Sarem FMurdoch Gordon KTibary AhmedWaits LiseNe PRhie ArangKoren SergeyPhillipy Adam MMcKay Stephanie DClarke Shannon MClark Emily LBrauning RudigerCockett Noelle EHammond John AHighland MaggieSafonova YanaSmith Timothy P LRosen Benjamin DMurdoch Brenda M - Adipogenic differentiation stands as a crucial pathway in the range of differentiation options for mesenchymal stem cells (MSCs), carrying significant importance in the fields of regenerative medicine and the treatment of conditions such as obesity and osteoporosis. However, the exact mechanisms that control the adipogenic differentiation of MSCs are not yet fully understood. - Source: PubMed
Publication date: 2024/08/29
Dai MiaomiaoHong WeishengOuyang Yi - Recent large-scale genome-wide association studies (GWAS) have started to identify potential genetic risk loci associated with risk of suicide; however, a large portion of suicide-associated genetic factors affecting gene expression remain elusive. Dysregulated gene expression, not assessed by GWAS, may play a significant role in increasing the risk of suicide death. We performed the first comprehensive genomic association analysis prioritizing brain expression quantitative trait loci (eQTLs) within regulatory regions in suicide deaths from the Utah Suicide Genetic Risk Study (USGRS). 440,324 brain-regulatory eQTLs were obtained by integrating brain eQTLs, histone modification ChIP-seq, ATAC-seq, DNase-seq, and Hi-C results from publicly available data. Subsequent genomic analyses were conducted in whole-genome sequencing (WGS) data from 986 suicide deaths of non-Finnish European (NFE) ancestry and 415 ancestrally matched controls. Additional independent USGRS suicide deaths with genotyping array data (n = 4657) and controls from the Genome Aggregation Database were explored for WGS result replication. One significant eQTL locus, rs926308 (p = 3.24e-06), was identified. The rs926308-T is associated with lower expression of RFPL3S, a gene important for neocortex development and implicated in arousal. Gene-based analyses performed using Sherlock Bayesian statistical integrative analysis also detected 20 genes with expression changes that may contribute to suicide risk. From analyzing publicly available transcriptomic data, ten of these genes have previous evidence of differential expression in suicide death or in psychiatric disorders that may be associated with suicide, including schizophrenia and autism (ZNF501, ZNF502, CNN3, IGF1R, KLHL36, NBL1, PDCD6IP, SNX19, BCAP29, and ARSA). Electronic health records (EHR) data was further merged to evaluate if there were clinically relevant subsets of suicide deaths associated with genetic variants. In summary, our study identified one risk locus and ten genes associated with suicide risk via gene expression, providing new insight into possible genetic and molecular mechanisms leading to suicide. - Source: PubMed
Publication date: 2023/10/04
Han SeonggyunDiBlasi EmilyMonson Eric TShabalin AndreyFerris ElliottChen DanliFraser AlisonYu ZheStaley MichaelCallor W BrandonChristensen Erik DCrockett David KLi Qingqin SWillour VirginiaBakian Amanda VKeeshin BrooksDocherty Anna REilbeck KarenCoon Hilary - Understanding the regulatory mechanisms of glioblastoma growth is crucial for developing novel therapies. In this study, the expression and function of zinc finger protein 501 (ZNF501) in human glioblastoma cells were characterized. ZNF501 was abundantly expressed in human glioblastoma cell lines U251, U118, U87, and U138. ZNF501 ablation in these cell lines caused inhibition of proliferation, sphere formation, and the expression of SOX2 and OCT4. Besides, ZNF501 ablation increased the sensitivity of these cell lines to Temozolomide but did not influence cell migration. Orthotopic implantation of U251 cells and U118 cells indicated that ZNF501 ablation suppressed glioblastoma cell proliferation and tumor formation in vivo. ZNF501 ablation induced down-regulation of Frizzled-6 (FZD6), a component of the Wnt signaling. Lentivirus-mediated FZD6 overexpression restored the proliferation, sphere formation, drug sensitivity, and SOX2 and OCT4 expression in these cell lines. ZNF501 ablation also incurred down-regulation of JNK phosphorylation which is an indicator of the non-canonical Wnt signaling, but did not change the expression of active β-catenin which is the hallmark of the canonical Wnt signaling. Inhibition of the non-canonical Wnt signaling abrogated the effects of ZNF501 and FZD6. Therefore, for the first time, we showed that ZNF501 is essential for the growth and stemness of glioblastoma cells possibly by maintaining FZD6 expression and the non-canonical Wnt signaling. - Source: PubMed
Publication date: 2022/06/08
Zheng HuWu LiuyangFan JingxinYuan Huisheng - Depression is the most prevalent mental disorder with substantial morbidity and mortality. Although genome-wide association studies (GWASs) have identified multiple risk variants for depression, due to the complicated gene regulatory mechanisms and complexity of linkage disequilibrium (LD), the biological mechanisms by which the risk variants exert their effects on depression remain largely unknown. Here, we perform a transcriptome-wide association study (TWAS) of depression by integrating GWAS summary statistics from 807,553 individuals (246,363 depression cases and 561,190 controls) and summary-level gene-expression data (from the dorsolateral prefrontal cortex (DLPFC) of 1003 individuals). We identified 53 transcriptome-wide significant (TWS) risk genes for depression, of which 23 genes were not implicated in risk loci of the original GWAS. Seven out of 53 risk genes (B3GALTL, FADS1, TCTEX1D1, XPNPEP3, ZMAT2, ZNF501 and ZNF502) showed TWS associations with depression in two independent brain expression quantitative loci (eQTL) datasets, suggesting that these genes may represent promising candidates. We further conducted conditional analyses and identified the potential risk genes that driven the TWAS association signal in each locus. Finally, pathway enrichment analysis revealed biologically pathways relevant to depression. Our study identified new depression risk genes whose expression dysregulation may play a role in depression. More importantly, we translated the GWAS associations into risk genes and relevant pathways. Further mechanistic study and functional characterization of the TWS depression risk genes will facilitate the diagnostics and therapeutics for depression. - Source: PubMed
Publication date: 2021/05/21
Li XiaoyanSu XiLiu JieweiLi HuijuanLi Ming Li WenqiangLuo Xiong-Jian