GATA6
- Known as:
- GATA6
- Catalog number:
- 000424A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GATA6
Related genes to: GATA6
- Gene:
- GATA6 NIH gene
- Name:
- GATA binding protein 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 18q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-11
- Date modifiied:
- 2016-10-05
Related products to: GATA6
Related articles to: GATA6
- Na -Ca exchanger 1 (NCX1), an antiporter that regulates the homeostasis of calcium and sodium ions contributes to neuroprotection elicited by ischemic preconditioning. In the brain, NCX1 is transcriptionally regulated by two gene promoters: NCX1-Br (brain) and NCX1-Ht (heart). Notably, the epigenetic mechanism involved in the methylation of cytosine (C) to form 5-methylcytosine (5mC) in neurons represses NCX1-Ht, but not NCX1-Br promoter activity. Importantly, hydroxylation of 5mC via ten eleven translocases (TET) enzymes leads to 5-hydroxymethylcytosine (5hmC), a marker of transcriptional activation. Herein, in ascorbic acid-treated SH-SY5Y cells TET3 isoform promoted 5hmC formation at NCX1-Ht promoter, but not at the level of NCX1-Br promoter, thus inducing NCX1 mRNA and protein up-regulation. Notably, TET3 physically interacted with the transcription factor GATA-binding factor 6 (GATA6), but not with RE1-silencing transcription factor (REST), and site-direct mutagenesis of GATA binding sites present on NCX1-Ht sequence blocked GATA6 and TET3 binding on NCX1 gene. Furthermore, GATA6 and TET3 protein levels were up-regulated in cortical neurons exposed to the neuroprotective hypoxic preconditioning (PC) stimulus followed by oxygen and glucose deprivation (OGD/Rx), that caused an increase of DNA hydroxymethylation on NCX1-Ht promoter, an effect not observed in neurons exposed to OGD/Rx alone. Collectively, this study showed that in neurons the exposure to PC followed by OGD/Rx 72 h elicited the formation of GATA6/TET3 complex that, by binding NCX1-Ht promoter, epigenetically activates NCX1 gene transcription. Given the NCX1 neuroprotective role in PC followed by OGD/Rx, activating this epigenetic pathway could be a potential therapeutic target for stroke treatment. - Source: PubMed
Publication date: 2026/05/13
Guida NatasciaRuggiero SilviaSerani AngeloSisalli Maria JosèMascolo LuigiSanguigno LucaFerrante AnnaCuomo OrnellaD'Apolito ElenaLaudati GiusyScorziello AntonellaPignataro GiuseppeAnnunziato LucioFormisano Luigi - An individual's host genetics influence its susceptibility to both COVID-19 and coronary artery disease (CAD). We analyzed large-scale GWAS datasets encompassing 7.7 million SNPs to identify shared genetic architecture between the two diseases. We identified 24 pleiotropic risk loci for both COVID-19 and CAD, with three loci (1p31.1, 8p21.3, and 18q11.2) showing strong evidence for a single shared causal variant. Loci in the 8p21.3 and 18q11.2 regions showed a bidirectional causal association: COVID-19 to CAD or vice versa, while the 1p31.1 locus only showed a CAD to COVID-19 unilateral casual association in a Mendelian randomization analysis (GSMR). A fine mapping analysis of the three loci identified three lead pleiotropic variants (rs7515509, rs8192330, and rs4800403). The variant rs7515509 was spatially associated with , and ; rs8192330 with , and several other genes; and rs4800403 with and . Transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) from COVID-19 patients validated proxitropic variants (rs8192330 and rs4800403) with distinct expression signatures and prioritized and as the likely causal genes. Overexpression of has been linked to the heme metabolism hallmark, disrupted iron distribution in COVID-19 patients with comorbid CAD, and subsequent stress erythropoiesis, oxidative stress, immunological dysfunction, and altered wound healing, while a lower expression of has been observed in the cytoplasmic translation and regulation of mRNA metabolism. In conclusion, we identified shared genetic components for COVID-19 and CAD and prioritized and as the likely causal genes for the observed shared genetic risk. COVID-19 may act as an acute stressor that unmask or accelerates underlying CAD. - Source: PubMed
Publication date: 2026/05/05
Ali Muhammad SarfrazHaider WaseemAziz SanaMohammad AnwaruddinManichaikul AniShi Weibin - The GATA family of zinc finger DNA-binding transcription factors plays a crucial role in regulating genes responsible for embryogenesis, cellular differentiation, and normal physiological development. This family comprises six members, designated as GATA1 to GATA6, with GATA4 being of particular significance due to its prominent tissue-specific functions. Mutations in GATA4 have been extensively linked with human congenital diseases affecting the heart, lungs, and reproductive system. It is regulated by post-translational modifications, notably phosphorylation at serine 105 by ERK and p38MAPK kinases. The expression and oncogenic/tumor-suppressive roles of GATA4 in cancer have sparked substantial research interest. GATA4 forms essential regulatory complexes with its family members, GATA5 and GATA6 during early myocardial development, and with transcriptional cofactors such as TBX5 and NKx2-5, underscoring its importance in maintaining cellular and molecular homeostasis. Emerging evidence highlights that dysregulated GATA4 expression contributes not only to developmental abnormalities but also to cancer progression, where it may exhibit oncogenic or tumor-suppressive functions depending on the tissue context. These dual roles highlight GATA4 as a crucial molecular node in pathways governing cell survival, proliferation, and tumorigenesis. Therefore, understanding the multifaceted biological implications of GATA4 is indispensable for identifying novel therapeutic targets. This review aims to comprehensively summarize the functional significance of GATA4 in the pathophysiology of developmental disorders and diverse cancers. - Source: PubMed
Publication date: 2026/05/07
Dharshini Loganathan Chandramani PriyaRasmi Rajan RadhaSakthivel Kunnathur MurugesanMuniandi Balakumar - The increase in incidence of early-onset pancreatic cancer (EOPC) is of concern and poorly understood. The aim of this study was to investigate the clinical outcomes of surgically resected patients with EOPC and the potential molecular heterogeneity between EOPC and late age-onset disease. - Source: PubMed
Dreyer Stephan BBryce AdamFroeling FiekeJackson ShannonSantana LeonorDickson Euan JCoats MariaMcKay ColinHolroyd DavidBiankin Andrew VJamieson Nigel BChang David K - Endometriosis (EMs) is a chronic gynaecological condition characterised by the ectopic growth of endometrial tissue; however, its molecular mechanisms remain insufficiently understood. Ferroptosis, an iron-dependent form of regulated cell death, has been suggested as a potential contributor to its pathogenesis. This study aimed to identify differentially expressed ferroptosis-related genes (DE-FRGs) in EMs through bioinformatics analysis and to explore their underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/04/30
Xu Jia-YanLiu Qin