ZNF675 antibody - N - terminal region (OAAB13375)
- Known as:
- ZNF675 (anti-) - N - terminal region (OAAB13375)
- Catalog number:
- oaab13375
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF675 antibody - terminal region (OAAB13375)
Related genes to: ZNF675 antibody - N - terminal region (OAAB13375)
- Gene:
- ZNF675 NIH gene
- Name:
- zinc finger protein 675
- Previous symbol:
- -
- Synonyms:
- TIZ, TBZF
- Chromosome:
- 19p12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-28
- Date modifiied:
- 2014-11-19
Related products to: ZNF675 antibody - N - terminal region (OAAB13375)
Related articles to: ZNF675 antibody - N - terminal region (OAAB13375)
- In this study, we investigated recurrent copy number variations (CNVs) in the 19p12 locus, which are associated with neurodevelopmental disorders. The two genes in this locus, ZNF675 and ZNF681, arose via gene duplication in primates, and their presence in several pathological CNVs in the human population suggests that either or both of these genes are required for normal human brain development. ZNF675 and ZNF681 are members of the Krüppel-associated box zinc finger (KZNF) protein family, a class of transcriptional repressors important for epigenetic silencing of specific genomic regions. About 170 primate-specific KZNFs are present in the human genome. Although KZNFs are primarily associated with repressing retrotransposon-derived DNA, evidence is emerging that they can be co-opted for other gene regulatory processes. We show that genetic deletion of ZNF675 causes developmental defects in cortical organoids, and our data suggest that part of the observed neurodevelopmental phenotype is mediated by a gene regulatory role of ZNF675 on the promoter of the neurodevelopmental gene Hes family BHLH transcription factor 1 (HES1). We also find evidence for the recently evolved regulation of genes involved in neurological disorders, microcephalin 1 and sestrin 3. We show that ZNF675 interferes with HES1 auto-inhibition, a process essential for the maintenance of neural progenitors. As a striking example of how some KZNFs have integrated into preexisting gene expression networks, these findings suggest the emergence of ZNF675 has caused a change in the balance of HES1 autoregulation. The association of ZNF675 CNV with human developmental disorders and ZNF675-mediated regulation of neurodevelopmental genes suggests that it evolved into an important factor for human brain development. - Source: PubMed
Lodewijk Gerrald Ade Geus MatthijsGuimarães Rita L F PJacobs Frank M J - How do transcriptomics vary in haploid human androgenote embryos at single cell level in the first four cell cycles of embryo development? - Source: PubMed
Vendrell Xde Castro PEscrich LGrau NGonzalez-Martin RQuiñonero AEscribá M JDomínguez F - Although parental genomes undergo extensive epigenetic reprogramming to be equalized after fertilization, whether they play different roles in human zygotic genome activation (ZGA) remains unknown. Here, we mapped parental transcriptomes by using human parthenogenetic (PG) and androgenetic (AG) embryos during ZGA. Our data show that human ZGA is launched at the 8-cell stage in AG and bi-parental embryos, but at the morula stage in PG embryos. In contrast, mouse ZGA occurs at the same stage in PG and AG embryos. Mechanistically, primate-specific ZNF675 with AG-specific expression plays a role in human ZGA initiated from paternal genome at the 8-cell stage. AG-specifically expressed LSM1 is also critical for human maternal RNA degradation (MRD) and ZGA. The allelic expressions of ZNF675 and LSM1 are associated with their allelically epigenetic states. Notably, the paternally specific expressions of ZNF675 and LSM1 are also observed in diploid embryos. Collectively, human ZGA is initiated from paternal genome. - Source: PubMed
Publication date: 2023/01/31
Yuan ShenliZhan JianhongZhang JingyeLiu ZhenboHou ZhenzhenZhang ChuanxinYi LizhiGao LeiZhao HanChen Zi-JiangLiu JiangWu Keliang - Although the environmental influences on infant attachment disorganization and security are well-studied, little is known about their heritability. Candidate gene studies have shown small, often non-replicable effects. In this study, we gathered the largest sample (N = 657) of ethnically homogenous, 14-month-old children with both observed attachment and genome-wide data. First, we used a Genome-Wide Association Study (GWAS) approach to identify single nucleotide polymorphisms (SNPs) associated with attachment disorganization and security. Second, we annotated them into genes (Versatile Gene-based Association Study) and functional pathways. Our analyses provide evidence of novel genes (HDAC1, ZNF675, BSCD1) and pathways (synaptic transmission, cation transport) associated with attachment disorganization. Similar analyses identified a novel gene (BECN1) but no distinct pathways associated with attachment security. The results of this first extensive, exploratory study on the molecular-genetic basis of infant attachment await replication in large, independent samples. - Source: PubMed
Publication date: 2015/05/05
Pappa IreneSzekely EszterMileva-Seitz Viara RLuijk Maartje P C MBakermans-Kranenburg Marian Jvan IJzendoorn Marinus HTiemeier Henning - Recent genome-wide association studies (GWAS) of chronic periodontitis (CP) offer rich data sources for the investigation of candidate genes, functional elements, and pathways. We used GWAS data of CP (n = 4,504) and periodontal pathogen colonization (n = 1,020) from a cohort of adult Americans of European descent participating in the Atherosclerosis Risk in Communities study and employed a MAGENTA approach (i.e., meta-analysis gene set enrichment of variant associations) to obtain gene-centric and gene set association results corrected for gene size, number of single-nucleotide polymorphisms, and local linkage disequilibrium characteristics based on the human genome build 18 (National Center for Biotechnology Information build 36). We used the Gene Ontology, Ingenuity, KEGG, Panther, Reactome, and Biocarta databases for gene set enrichment analyses. Six genes showed evidence of statistically significant association: 4 with severe CP (NIN, p = 1.6 × 10(-7); ABHD12B, p = 3.6 × 10(-7); WHAMM, p = 1.7 × 10(-6); AP3B2, p = 2.2 × 10(-6)) and 2 with high periodontal pathogen colonization (red complex-KCNK1, p = 3.4 × 10(-7); Porphyromonas gingivalis-DAB2IP, p = 1.0 × 10(-6)). Top-ranked genes for moderate CP were HGD (p = 1.4 × 10(-5)), ZNF675 (p = 1.5 × 10(-5)), TNFRSF10C (p = 2.0 × 10(-5)), and EMR1 (p = 2.0 × 10(-5)). Loci containing NIN, EMR1, KCNK1, and DAB2IP had showed suggestive evidence of association in the earlier single-nucleotide polymorphism-based analyses, whereas WHAMM and AP2B2 emerged as novel candidates. The top gene sets included severe CP ("endoplasmic reticulum membrane," "cytochrome P450," "microsome," and "oxidation reduction") and moderate CP ("regulation of gene expression," "zinc ion binding," "BMP signaling pathway," and "ruffle"). Gene-centric analyses offer a promising avenue for efficient interrogation of large-scale GWAS data. These results highlight genes in previously identified loci and new candidate genes and pathways possibly associated with CP, which will need to be validated via replication and mechanistic studies. - Source: PubMed
Publication date: 2014/07/23
Rhodin KDivaris KNorth K EBarros S PMoss KBeck J DOffenbacher S