Ask about this productRelated genes to: p66alpha antibody
- Gene:
- GATAD2A NIH gene
- Name:
- GATA zinc finger domain containing 2A
- Previous symbol:
- -
- Synonyms:
- p66alpha
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-31
- Date modifiied:
- 2014-11-19
Related products to: p66alpha antibody
Related articles to: p66alpha antibody
- The zinc finger MYND-type containing 8 protein (ZMYND8) is a chromatin reader that regulates neuronal gene expression by controlling the microtubule-associated protein tau (MAPT) locus. Here, we investigate how ZMYND8 regulates expression of the long non-coding RNA MAPT213 through its interaction with GATA zinc finger domain containing 2A (GATAD2A), a component of the Nucleosome Remodelling and Deacetylase (NuRD) complex. ZMYND8 exhibits opposite regulatory effects on protein-coding MAPT and non-coding MAPT213 transcripts in a manner dependent on its MYND domain, promoting MAPT expression while suppressing MAPT213 levels. Chromatin immunoprecipitation experiments demonstrated that ZMYND8 specifically recruits GATAD2A to the MAPT213 internal regulatory region, establishing a direct link between protein binding and transcriptional control. We determined the crystal structure of the ZMYND8 coiled-coil MYND domain at high resolution, revealing a homodimeric architecture. The MYND domain specifically recognizes GATAD2A through direct interaction with proline-rich motifs in GATAD2A's central region. Structure-function analysis identified critical binding interface residues, while quantitative measurements revealed moderate-affinity interactions enhanced through multivalent binding mechanisms. These findings establish the molecular basis for ZMYND8-mediated recruitment of chromatin remodeling complexes to specific genomic loci and provide a structural framework for understanding transcriptional regulation of MAPT213. - Source: PubMed
Publication date: 2026/04/16
Srivastava Dushyant KumarNandi SandhikKarmakar AvradeepDas ChandrimaRoy Siddhartha - The observational studies confirmed the high prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) in patients with Type 2 diabetes mellitus (T2DM), but whether this reflects a shared genetic etiology and exists underlying causal relationships remains unknown. Here, we utilized the largest scale cross-trait analysis from genome-wide association studies (GWASs) to investigate the shared genetic architecture and found a significant genetic correlation between T2DM and MASLD. Subsequently, we identified 581 shared risk single-nucleotide polymorphisms (SNPs) and observed consistent patterns of tissue-specific heritability enrichment in embryonic stem cells, stomach, kidney, large and small intestine, and pancreas. Of the six highly shared risk SNPs (rs7203132, rs11642015, rs58542926, rs6857, rs10404726, and rs738408), we further systematically performed regional and functional analysis. Using Mendelian randomization (MR), we discovered significant evidence for a positive causal effect with no reverse causality of T2DM on MASLD and further explained what causes causality to occur. Finally, we used an orthogonal strategy to provide genetic evidence, highlighting 11 possible comorbidity targets, most of which are located on Chromosomes 19 or 22 with five on 19p13.11, such as NCAN, MAU2, GATAD2A, TM6SF2, and GMIP. Our study sheds insights into the informed biology of comorbidity and reveals their shared genetic factors and potential drug targets. - Source: PubMed
Publication date: 2026/04/09
Zhu ZijunLi HailongWang XinChen XinyuCheng Liang - O-GlcNAc modification is a key cellular signal, but its role in regulating senescence-associated transcription remains poorly understood. Here, we apply a time-resolved chemical genomics strategy to map dynamic O-GlcNAc chromatin-associated proteins (OCPs) during oncogene-induced senescence (OIS) in primary human fibroblasts. Chromatin O-GlcNAc modification continues to accumulate, while 1,987 senescence-associated OCPs undergo dynamic shifts in genomic occupancy across diverse epigenetic chromatin states and display bimodal regulatory activities within the 3,466-gene senescence transcriptome. O-GlcNAc facilitates the formation of dual-function complexes: TF-SWI/SNF activates senescence-associated secretory phenotype (SASP) genes at promoters, whereas NuRD enforces the repression of cell-cycle regulators at enhancers. Furthermore, we identify O-GlcNAc modified JUN and GATAD2A as key regulators of OIS phenotypes in both in vitro and in vivo models of senescence-driven tumorigenesis. These findings reveal dynamic regulation and chromatin organization principles of O-GlcNAc-related epigenetic factors, providing insights into cellular senescence and potential therapeutic strategies. - Source: PubMed
Publication date: 2026/01/08
Zhang NanaZhao RanZhong XiaominDong QianLiu YajieYu KairanHan LiruiMeng FanxuWu JiaxuanChen QiushiLi XuechenChen QingbinZhang KerenHuang HuangZhang JianingWu SijinRen YanWang WeiLiu Yubo - Epidemiological evidence suggests a link between schizophrenia (SCZ) and increased breast cancer (BC) risk, but the genetic mechanisms remain unclear. Exploring their shared genetic susceptibility may help reveal the basis of this comorbidity. - Source: PubMed
Publication date: 2025/12/09
Zhang MinWu YongliQin Yujie - Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy, yet the transcriptional hierarchies linking endocrine signaling to tumor progression remain poorly defined. Here, we integrated gene-expression profiles from two independent cohorts (TCGA-THCA and GSE33630) to identify consensus transcriptional master regulators (TMRs) driving PTC. After normalization and differential expression analysis, we reconstructed regulon networks with ARACNe-AP, inferred TMR activity using VIPER, and integrated evidence across datasets via Fisher's meta-analysis. This cross-cohort strategy yielded 50 shared TMRs, predominantly from the Zinc Finger, Forkhead, ETS, and nuclear receptor families. Network topology highlighted , , , , and as upstream regulators controlling other TMRs. Functional enrichment revealed activation of NOTCH, MAPK, PI3K, and TGF-β signaling and enrichment of early and late estrogen-response programs, uncovering a noncanonical role of in TGF-β signaling. Together, these findings delineate the transcriptional and hormonal circuitry underlying thyroid tumorigenesis, providing a regulatory framework for biomarker-driven therapies based on network activity states. - Source: PubMed
Publication date: 2025/11/20
Tapia-Carrillo DianaZambada-Moreno OctavioHernández-Lemus EnriqueTovar Hugo