GATA6

GATA6

A gene on chromosome 18q11.1-q11.2 that encodes a member of the GATA family of zinc finger transcription factors, which is thought to play a key role in regulating proliferation and terminal differentiation.
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PNDM is a genetically heterogeneous disorder due to mutations in 23 different genes described to date: KCNJ11, ABCC8, FOXP3, GCK, PDX1, pancreas-specific transcription factor 1A (PTF1A), EIF2AK3, SLC2A2, GATA6, GATA4, SLC19A2, WFS1, NEUROD1, NEUROG3, RFX6, LRBA, NKX2-2, MNX1, IER3IP1, INS, S T A T 3 , GLIS3 and HNF1B (3,4,5,6,7,8,9).
Among them, we found the principal components of major regulatory clusters, involving inflammatory responses (IFNy, IL6, several members of the interleukin 1 pathway, including ILIA, IL1B, IL1RN, and the TNF pathway members TNF, TNFAIP6, TNFSF15, TNFRSF9), angiogenesis (CXCL10, PTGS2), immune regulation (CD80, CD274, CSF3, IL23R), leukocyte chemotaxis (CCL2, CCL3, CCL4, CCL20, CCL23, CCL3L3, CXCL1, CXCL2, CXCL5, CXCL9), transcriptional regulation (EGR1, GATA6, HEY1), proliferation (CDKN2B, FGFR1), adhesion (ITGB8), extracellular matrix remodeling (ADAMTS4), cell-cell communication (GJB2), cell signaling (EDNRB, IRS1, RIN2), ion transmembrane transport (KCNJ2, CLIC4), and response to oxidative stress (SOD2).
Individuals with other syndromic forms of neonatal diabetes have neurocognitive impairments in addition to other multisystem features, e.g., GATA6 mutations cause cardiac defects, pancreatic exocrine insufficiency, gut abnormalities, and hypothyroidism/hypopituitarism [93].
Another example is the large peritoneal macrophage population that relies on dietary retinoic acid induction of the transcription factor Gata6 to develop and survive [11].
Lest we think that MDx of exhaled breath is limited to DNA, a study by Mehta et al (6) examined mRNA expression ratios of two markers (GATA6 and NKX2-1) in EBC from lung cancer and control populations.
Mutations in NKX2-5 (5q35.1), GATA4 (8q23.1), ZFPM2 (8q23.1), GATA6 (18q11.2), GDF1 (19p13.11), JAG1 (20p12.2), and TBX1 (22q11.21) have been reported in sporadic cases with tetralogy of Fallot; however, interaction of these genes and FMR1 gene has never been reported [49].
Overexpression of KRAS enhances the transcription of NOX1 through RAF/ MEK/ERK-dependent phosphorylation of the transcription factor GATA6 [66].
MiR-145 showed its negative effect in isoproterenol-induced cellular hypertrophy via regulation of the expression of GATA binding protein 6 (GATA6) [21, 22].
Although iPSC-CMs express relevant ion channel genes (SCN5A, KCNJ2, CACNA1C, KCNQ1, and KCNH2), structural genes (MYH6, MYLPF, MYBPC3, DES, TNNT2, and TNNI3), and transcription factors (NKX2.5, GATA4, and GATA6) [77], they differ from adult ventricular cardiomyocytes in a number of properties.
Targets prediction revealed that miR-92a targeted both GATA family of zinc finger transcription factor GATA-binding factor 6 (GATA6) and insulin receptor substrate proteins 2 (IRS-2).
Although this is not necessarily true, there exist at least three important maternal transcription factors and cofactors that play critical roles in fate determination: [beta]-catenin, (28,29) Gata.a (30,31) (a possible ortholog of vertebrate GATA4, GATA5, and GATA6; the original name was Gata-a), and the Zic-like protein Macho-1/Zic-r.a (Macho-1 is the original name and Zic-r.a is the new name).
Synergistic Induction of DOC-2/DAB2 Gene Expression in Transitional Cell Carcinoma in the Presence of GATA6 and Histone Deacetylase Inhibitor.