Ask about this productRelated genes to: ZNF596 antibody
- Gene:
- ZNF596 NIH gene
- Name:
- zinc finger protein 596
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-01
- Date modifiied:
- 2014-11-19
Related products to: ZNF596 antibody
Related articles to: ZNF596 antibody
- Breast cancer comprises distinct molecular subtypes, including HER2-enriched, Luminal A, Luminal B, and triple-negative breast cancer (TNBC), each driven by distinct transcriptional programs and clinical behavior. However, the regulatory roles of zinc-finger transcription factors (ZNFs) underlying these subtype-specific programs remain incompletely defined. We performed a systematic RNA-sequencing-based comparative transcriptomic analysis across all major subtypes, incorporating differential expression analysis, pathway enrichment, protein-protein interaction network reconstruction, promoter motif scanning, and exploratory variant analysis to infer ZNF-centered regulatory architectures. HER2⁺ and Luminal B tumors exhibited the highest degree of transcriptional disruption, whereas Luminal A displayed comparatively limited deregulation. This analysis identified four subtype-specific ZNF hubs, MAZ (TNBC), ZNF596 (HER2⁺), ZNF366 (Luminal B), and ZNF671 (Luminal A), forming compact regulatory modules supported by promoter motif enrichment, indicative of putative transcription factor binding potential. Cross-subtype pathway analysis revealed conserved enrichment of Krüppel-associated box (KRAB) zinc-finger-mediated repression of endogenous retroelements, suggesting a shared epigenetic mechanism of transcriptional control. Interpretation is bounded by transcriptome-based regulatory inference without functional perturbation and by the absence of longitudinal or treatment-response data, limiting definitive causal attribution. Nonetheless, these findings establish a structured regulatory framework highlighting ZNF-driven transcriptional hierarchies across breast cancer subtypes. - Source: PubMed
Publication date: 2026/02/17
Ali MuhammadSaqib ManahilAli ZaeemRashid Sajid - Given the differential risk of type 1 diabetes (T1D) in offspring of affected fathers versus affected mothers and our observation that T1D cases have differential DNA methylation near the imprinted gene compared to controls, we examined whether methylation near mediates the association between T1D family history and T1D risk. In a nested case-control study of 87 T1D cases and 87 controls from the Diabetes Autoimmunity Study in the Young, we conducted causal mediation analyses at 12 region CpGs to decompose the effect of family history on T1D risk into indirect and direct effects. These effects were estimated from two regression models adjusted for the human leukocyte antigen DR3/4 genotype: a linear regression of family history on methylation (mediator model) and a logistic regression of family history and methylation on T1D (outcome model). For 8 of the 12 CpGs, we identified a significant interaction between T1D family history and methylation on T1D risk. Accounting for this interaction, we found that the increased risk of T1D for children with affected mothers compared to those with no family history was mediated through differences in methylation at two CpGs (cg27351978, cg00565786) in the region, as demonstrated by a significant pure natural indirect effect (odds ratio (OR) = 1.98, 95% confidence interval (CI): 1.06-3.71) and nonsignificant total natural direct effect (OR = 1.65, 95% CI: 0.16-16.62) (for cg00565786). In contrast, the increased risk of T1D for children with an affected father or sibling was not explained by DNA methylation changes at these CpGs. Results were similar for cg27351978 and robust in sensitivity analyses. Lastly, we found that DNA methylation in the region was associated (<0:05) with gene expression of nearby protein-coding genes , , , and . Results indicate that the maternal protective effect conferred through exposure to T1D may operate through changes to DNA methylation that have functional downstream consequences. - Source: PubMed
Publication date: 2023/09/11
Johnson Randi KIreton Amanda JCarry Patrick MVanderlinden Lauren ADong FranRomero AlexJohnson David RGhosh DebashisYang FanFrohnert BrigitteYang Ivana VKechris KaterinaRewers MarianNorris Jill M - Genome-wide association studies (GWAS) have been used as an effective tool to understand the genetics of complex traits such as gastrointestinal parasite (GIP) resistance. The aim of this study was to understand the genetics of gastrointestinal parasite (nematodes, , ) resistance in Akkaraman sheep by performing genomic heritability estimations and conducting GWAS to uncover responsible genomic regions. This is one of the first studies to examine the genetic resistance of Akkaraman sheep to the tapeworm parasite. The samples from 475 animals were genotyped using the Axiom 50K Ovine Genotyping Array. Genomic heritability estimates ranged from 0.00 to 0.34 for parasite resistance traits. This indicates that measured phenotypes have low to moderate heritability estimates. A total of two genome-wide significant SNP associated with and genes and 10 chromosome-wide significant SNPs related with 10 genes namely , , , , , , , , , and were suggested as candidates for parasite resistance traits. The majority of these candidate genes were involved in several basic biological processes that are essential and important for immune system functions and cellular growth; specifically, inflammatory responses, cellular transport, cell apoptosis, cell differentiation, histone de-acetylation, and endocytosis. These results have implications for animal breeding program studies due to the effect that the genetic background has on parasite resistance, which underlies many productive, health, and wellness-related traits. - Source: PubMed
Publication date: 2022/11/22
Arzik YunusKizilaslan MehmetWhite Stephen NPiel Lindsay M WÇınar Mehmet Ulaş - N6-methyladenosine (m6A) modification holds an important position in tumorigenesis and metastasis because it can change gene expression and even function in multiple levels including RNA splicing, stability, translocation and translation. In present study, we aim to conducted comprehensive investigation on m6A RNA methylation regulators and m6A-related genes in pancreatic cancer and their association with survival time. - Source: PubMed
Geng YanGuan RenguoHong WeifengHuang BowenLiu PeizhenGuo XiaohuaHu ShixiongYu MinHou Baohua - Long non-coding RNAs (lncRNAs) are critical regulators in cancer. However, the involvement of lncRNAs in TGF-β-regulated tumorigenicity is still unclear. Here, we identify TGF-β-activated lncRNA LINC00115 as a critical regulator of glioma stem-like cell (GSC) self-renewal and tumorigenicity. LINC00115 is upregulated by TGF-β, acts as a miRNA sponge, and upregulates ZEB1 by competitively binding of miR-200s, thereby enhancing ZEB1 signaling and GSC self-renewal. LINC00115 also promotes ZNF596 transcription by preventing binding of miR-200s to the 5'-UTR of ZNF596, resulting in augmented ZNF596/EZH2/STAT3 signaling and GBM tumor growth. Inhibition of EZH2 by genetic approaches or a small molecular inhibitor markedly suppresses LINC00115-driven GSC self-renewal and tumorigenicity. Moreover, LINC00115 is highly expressed in GBM, and LINC00115 expression or correlated co-expression with ZEB1 or ZNF596 is prognostic for clinical GBM survival. Our work defines a critical role of LINC00115 in GSC self-renewal and tumorigenicity, and suggests LINC00115 as a potential target for GBM treatment. - Source: PubMed
Publication date: 2019/10/10
Tang JianmingYu BoLi YanxinZhang WeiweiAlvarez Angel AHu BoCheng Shi-YuanFeng Haizhong