| 1998 |
GATA6 lies upstream of HNF4 in a transcriptional cascade regulating visceral endoderm differentiation; GATA6-null mice lack HNF4 expression in the endoderm, and forced GATA6 expression activates the HNF4 promoter in non-endodermal cells. GATA6-null embryoid bodies fail to form a visceral endoderm layer and lack expression of GATA4, AFP, and HNF3beta. |
Gene targeting (GATA6-null ES cells and mice), embryoid body differentiation, promoter activation assay, chimeric mouse analysis |
Genes & development |
High |
9832509
|
| 2001 |
Overexpression of GATA6 in cardiomyocytes is sufficient to induce hypertrophic growth (increased cell surface area, sarcomeric organization, protein accumulation), and a dominant-negative GATA4-engrailed repressor blocks GATA6-directed transcriptional responses and agonist-induced hypertrophy, demonstrating that GATA6 is a necessary mediator of cardiomyocyte hypertrophy. |
Recombinant adenovirus overexpression in cardiomyocytes, dominant-negative fusion protein (GATA4-engrailed), transgenic mouse overexpression, cell surface area and protein accumulation measurements |
The Journal of biological chemistry |
High |
11356841
|
| 2002 |
GATA6 is required for differentiation of alveolar epithelial type 1 cells in the distal lung; dominant-negative GATA6-Engrailed expression abolishes type 1 cells, increases Foxp2, and attenuates surfactant protein C expression. GATA6 can trans-activate the aquaporin-5 promoter, indicating direct transcriptional control of AT1-specific genes. |
Dominant-negative transgenic mice (GATA6-Engrailed driven by SP-C promoter), promoter trans-activation assay |
Development (Cambridge, England) |
High |
11959831
|
| 2004 |
Endoderm differentiation and endoderm-specific gene expression (including laminin 1 subunits) in embryoid bodies is controlled by FGF-induced GATA6; GATA6-transformed Lamc1-null endoderm-like cells show that laminin 1 in the basement membrane subsequently induces epiblast differentiation. |
GATA6 overexpression in ES cells, embryoid body differentiation, pharmacological inhibitors (dominant-negative), gene expression analysis |
Development (Cambridge, England) |
Medium |
15456727
|
| 2006 |
Gata6, but not Gata4, physically interacts with Nkx2.2 (an essential islet transcription factor). Dominant-negative Gata6-Engrailed expression in the pancreatic epithelium causes pancreatic agenesis or severe reduction of all pancreatic cell types, demonstrating Gata6 is an important regulator of pancreas specification. |
Co-immunoprecipitation (physical interaction with Nkx2.2), dominant-negative Gata6-Engrailed transgenic mice, histological analysis |
Developmental biology |
Medium |
16887115
|
| 2006 |
Compound heterozygosity for GATA4 and GATA6 null alleles causes embryonic lethality with cardiovascular defects (thin-walled myocardium, septal defects), reduced cardiomyocyte proliferation, and downregulation of MEF2C and beta-myosin heavy chain, revealing a dosage threshold for GATA4/GATA6 activity in cardiovascular gene expression. |
Compound heterozygous mouse genetics, histology, gene expression analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
16847256
|
| 2008 |
Gata6 regulates the temporal appearance and number of bronchioalveolar stem cells (BASCs) by suppressing canonical Wnt signaling; loss of Gata6 increases canonical Wnt signaling and causes precocious BASC expansion. Gata6 regulates expression of the non-canonical Wnt receptor Fzd2, and increased Fzd2 or decreased beta-catenin rescues lung epithelial defects in Gata6 mutants. |
Conditional Gata6-null lung epithelium mice, genetic rescue (Fzd2 expression, beta-catenin reduction), Wnt signaling reporter assays, postnatal Gata6 deletion |
Nature genetics |
High |
18536717
|
| 2008 |
Dynamic GATA6 expression distinguishes parietal endoderm (GATA6+) from visceral endoderm (GATA6 lost by E5.5). GATA6-null embryos fail to form a morphologically recognizable primitive endoderm layer, establishing GATA6 as essential for primitive endoderm formation at an earlier stage than previously recognized. |
Immunofluorescence, in situ hybridization, GATA6-null mouse embryo analysis |
Developmental dynamics |
Medium |
18816845
|
| 2008 |
GATA6 and FOXA2 directly bind to the Wnt6 promoter and activate its transcription, linking GATA6 to canonical WNT-β-catenin pathway activation during primitive endoderm formation in F9 teratocarcinoma cells. |
Chromatin immunoprecipitation, luciferase reporter assay, overexpression of Gata6 and Foxa2 in F9 cells |
Stem cells and development |
Medium |
22607194
|
| 2008 |
GATA6 activates calreticulin gene transcription by binding to site 1 on the calreticulin promoter (shown by EMSA and ChIP), while Evi-1 represses calreticulin and antagonizes GATA6-mediated activation at the same site. |
EMSA, chromatin immunoprecipitation, site-specific mutagenesis, reporter assays in neonatal cardiomyocytes and fibroblasts |
Biochemistry |
Medium |
18303859
|
| 2009 |
siRNA-mediated reduction of GATA6 in human ovarian surface epithelial cells causes nuclear envelope deformation, failure of cytokinesis, and formation of polyploid/aneuploid cells. Loss of the nuclear envelope protein emerin mediates these consequences; direct siRNA suppression of emerin phenocopies GATA6 loss. |
siRNA knockdown, flow cytometry, immunofluorescence, nuclear morphology analysis |
Molecular and cellular biology |
Medium |
19581290
|
| 2012 |
Simultaneous pancreas-specific deletion of both Gata4 and Gata6 causes severe pancreatic agenesis due to failure of progenitor cell proliferation, defects in branching morphogenesis, and loss of CPA1+ and NEUROG3+ progenitor differentiation; single deletion of either factor yields only mild defects that resolve postnatally. |
Conditional double knockout mice (Pdx1-Cre; Gata4fl/fl; Gata6fl/fl), histology, immunostaining, gene expression |
The Journal of clinical investigation |
High |
23006325 23006330
|
| 2013 |
Endothelial GATA-6 directly transcriptionally regulates genes controlling vascular tone (endothelin-1, eNOS) and pro-inflammatory genes (CX3CL1, PAI-1, RhoB). Endothelial-specific Gata6 knockout mice spontaneously develop elevated pulmonary artery pressure and increased vessel muscularization, with innate immune cell infiltration. |
Endothelial-specific Gata6 conditional KO mice, pulmonary artery pressure measurement, histology, gene expression analysis |
The American journal of pathology |
Medium |
23583651
|
| 2014 |
GATA6 levels regulate timing and speed of primitive endoderm (PrE) lineage commitment in the inner cell mass; GATA6 is necessary for PrE specification by FGF signaling; quantitative single-cell imaging shows that absence of GATA6 completely abolishes PrE and that GATA6 levels interact with NANOG and FGF/ERK to determine ICM fate. |
Quantitative single-cell-resolution image analysis, GATA6 hypomorphic and null embryos, FGF/ERK pathway manipulation |
Developmental cell |
High |
24835466
|
| 2014 |
In mouse ICM, absence of GATA6 causes all cells to adopt epiblast identity, while absence of NANOG causes all cells to adopt PrE identity; these findings support a tristable regulatory network model where ERK signaling and concentrations of Nanog, Gata6, Fgf4, and Fgfr2 control ICM cell fate. |
Gata6-null and Gata6+/- embryo analysis, mathematical modeling, FGF/Erk pathway manipulation |
Development (Cambridge, England) |
Medium |
25209243
|
| 2014 |
GATA6 directly enhances LGR5 expression, and miR-363 downregulates GATA6 thereby suppressing LGR5 and colorectal cancer tumourigenicity. The miR-363-GATA6-LGR5 axis is required for colorectal cancer tumorigenicity. |
Overexpression/knockdown assays, luciferase reporter assay (miR-363 targeting GATA6 3'UTR), in vivo xenograft |
Nature communications |
Medium |
24452072
|
| 2014 |
GATA6 and GATA4 maintain pancreatic endoderm identity in part by repressing hedgehog signaling; in Gata4/Gata6 double-knockout pancreatic progenitors, hedgehog pathway components are ectopically upregulated, and GATA4/GATA6 can repress transcription through the Shh endoderm-specific enhancer MACS1, requiring GATA-binding sites within this enhancer. |
Double conditional KO mice (pDKO), reporter assay with MACS1 enhancer, GATA binding site mutagenesis |
Development (Cambridge, England) |
Medium |
26932670
|
| 2014 |
GATA6 is a crucial regulator of Shh expression in the hindlimb bud; conditional Gata6 deletion from developing limbs causes ectopic Shh expression and preaxial polydactyly, and forced GATA6 expression represses Shh. GATA6 binds to regulatory elements of Shh and Gli1 in limb bud chromatin and represses their expression synergistically with FOG co-factors. Loss of Shh in Gata6-null limbs prevents polydactyly, placing GATA6 upstream of Shh. |
Conditional Gata6 KO (Prx1-Cre), forced Gata6 expression, ChIP, luciferase reporter assay, genetic epistasis (Shh/Gata6 double conditional KO) |
PLoS genetics |
High |
24415953
|
| 2015 |
Gata6 is sufficient to initiate reprogramming of multiple cell types (pluripotent and differentiated neural cells) to induced extraembryonic endoderm stem cells. ChIP-seq shows GATA6 enrichment near both pluripotency and endoderm genes, functioning as a direct repressor of pluripotency genes (Nanog, Esrrb, Sox2, Oct4) and activator of ExEn genes in a stepwise manner. |
Inducible Gata6 expression, cell reprogramming assays, ChIP-seq, transcriptional profiling |
Genes & development |
High |
26109048
|
| 2015 |
Gata6 maintains acinar differentiation and suppresses KrasG12V-driven pancreatic tumorigenesis; ChIP-seq and RNA-seq show that GATA6 directly represses the EGFR pathway and inflammatory pathways in the pancreas; Gata6 ablation renders acinar cells more sensitive to KRas(G12V) and accelerates tumor development. |
Genetically engineered mouse models, ChIP-seq, RNA-seq, GATA6 silencing in human PDAC cells |
Gut |
High |
25596178
|
| 2016 |
GATA6 inhibits epithelial-mesenchymal transition (EMT) in pancreatic cancer cells in vitro and cell dissemination in vivo; GATA6 ChIP-seq and RNA-seq demonstrate direct transcriptional regulation of EMT-related genes and indirect regulation through other EMT transcription factors. |
GATA6 silencing and overexpression in PDAC cell lines, ChIP-seq, RNA-seq, in vivo dissemination assay |
Gut |
High |
27325420
|
| 2016 |
Gata6 controls the renewal of rapidly proliferating hair follicle matrix progenitor cells by protecting against DNA damage associated with proliferation; Gata6 stimulates Edaradd expression and NF-κB pathway activation, and Edaradd rescues DNA damage, cell survival, proliferation, and MCM10 expression in Gata6-null keratinocytes. |
Conditional Gata6 KO mice, cultured keratinocyte rescue experiments with Edaradd, DNA damage assays, gene expression analysis |
The EMBO journal |
Medium |
27908934
|
| 2017 |
Gata6 controls the identity of the sebaceous duct lineage and specifies a lineage switch between sebocytes and SD cells; during wound healing, differentiated Gata6+ cells migrate from the sebaceous duct into the interfollicular epidermis and dedifferentiate, acquiring long-term self-renewal ability and multilineage differentiation capacity. |
Conditional Gata6 KO mice, lineage tracing, live imaging, clonogenic assays |
Nature cell biology |
High |
28504705
|
| 2017 |
GATA6 is required for normal insulin biosynthesis and secretion in adult β-cells; pancreas-specific Gata6 inactivation causes glucose intolerance, decreased insulin content, impaired insulin secretion, and ultrastructural abnormalities in β-cells. Pdx1 expression in adult β-cells depends on GATA-binding sites, and GATA6 loss greatly affects β-cell-specific gene expression. |
Pancreas-specific Gata6 KO mice, glucose tolerance testing, insulin secretion assays, electron microscopy, transgenic reporter mice with GATA site mutations |
Diabetes |
High |
29263149
|
| 2017 |
GATA6 and Sp1 interact and cooperatively activate Aqp5 transcription via histone H3 acetylation; GATA6 competes with HDAC3 for Sp1 binding, and p300 modulates H3 acetylation through interactions with GATA6/Sp1. GATA6 knockdown decreases AQP5 expression in alveolar epithelial cells. |
siRNA knockdown, HDAC inhibitor treatment, Co-IP (GATA6/Sp1/p300/HDAC3 interactions), ChIP for histone acetylation, reporter assays |
Scientific reports |
Medium |
28615712
|
| 2018 |
Phosphorylation of GATA6 at a conserved serine residue (S264) by Erk1/2 is required for GATA6 to activate its own promoter and drive a positive feedback loop for primitive endoderm differentiation; S264 mutations drastically impair GATA6's ability to activate its own promoter in ES cells. |
Gata6-H2BGFP knock-in mouse, ES cell differentiation, site-directed mutagenesis of S264, promoter activation assay |
Developmental biology |
High |
29454706
|
| 2018 |
Gata6 haploinsufficiency causes highly penetrant right-left-type bicuspid aortic valve in mice. Mechanistically, Gata6 haploinsufficiency disrupts valve remodeling and extracellular matrix composition through dysregulation of MMP9. Cell-specific inactivation reveals that GATA6 is required specifically in secondary heart field (Isl-1-positive) myocytes, not endothelial or neural crest cells, for aortic valve formation. |
Gata6 heterozygous mice, cell-specific conditional KO (Isl-1-Cre, endothelial-Cre, neural crest-Cre), MMP9 expression analysis, human GWAS validation |
Circulation |
High |
29567669
|
| 2018 |
In endometriosis, GATA6 is necessary for CYP17A1-mediated conversion of progesterone to androstenedione in endometriotic cells, and simultaneous expression of both GATA6 and NR5A1 is required and sufficient to activate all five steroidogenic genes (HSD3B2, CYP17A1, CYP19A1 and others) and estradiol production in normal endometrial stromal cells. |
Ectopic expression and siRNA knockdown of GATA6 and NR5A1 in endometrial and endometriotic stromal cells, estradiol ELISA, RT-qPCR, western blot |
Reproductive sciences |
Medium |
29402198
|
| 2019 |
GATA6 cooperates with EOMES/SMAD2/3 to regulate cardinal endoderm gene expression at the genome-wide level; GATA6-null human PSCs fail to enter the definitive endoderm lineage, while heterozygous cells show modest DE reduction, explaining the human-specific pancreatic agenesis with heterozygous GATA6 mutations. |
Gene-edited and patient-derived hPSCs, directed differentiation, ChIP-seq (GATA6, EOMES, SMAD2/3), RNA-seq, flow cytometry |
Stem cell reports |
High |
30629940
|
| 2019 |
GATA6 directly upregulates CD137L (TNFSF9) expression in cutaneous T-cell lymphoma cells by binding to its promoter; GATA6 overexpression in CTCL is driven by DNA hypomethylation and histone acetylation, and GATA6 inhibition decreases CTCL cell survival and in vivo growth. |
ChIP assay, luciferase reporter assay, shRNA knockdown, flow cytometry, in vivo mouse xenograft |
Blood |
Medium |
30194255
|
| 2019 |
GATA6 directly transcribes miR-520b (shown by luciferase reporter and ChIP assays), and miR-520b suppresses CREB1, establishing a GATA6/miR-520b/CREB1 axis that suppresses gastric cancer cell migration and metastasis. |
Luciferase reporter assay, ChIP, overexpression/knockdown, in vivo metastasis model |
Cell death & disease |
Medium |
30674866
|
| 2019 |
GATA6 directly binds the promoter of the PKM gene and regulates PKM2 transcription; GATA6 silencing in HCC cells promotes glycolytic metabolism, EMT, tumorigenicity, and self-renewal via PKM2 upregulation. |
ChIP assay, gene knockdown and overexpression, metabolic assays (glucose uptake), in vivo tumorigenicity |
International journal of cancer |
Medium |
30834518
|
| 2019 |
GATA6 physically interacts with LOXL2 (the scavenger receptor cysteine-rich domain of LOXL2 interacts with GATA6), and this complex promotes VEGFA mRNA expression and protein secretion, driving angiogenesis and tube formation in cholangiocarcinoma. |
Co-immunoprecipitation, western blot, RT-qPCR, ELISA, tube formation assay, in vivo xenograft |
International journal of oncology |
Medium |
31322171
|
| 2019 |
Gata4 directly represses Gata6 transcription through responsive repressive sites within 1 kb upstream of the Gata6 transcription start site, shown by ChIP-qPCR and luciferase reporter assay; enhanced Gata6 expression in Gata4 heterozygous SHF cells contributes to outflow tract defects. |
ChIP-qPCR, luciferase reporter assay, Gata4 heterozygous mouse model, gene expression analysis |
PLoS genetics |
Medium |
31120883
|
| 2020 |
GATA6 is a pioneer factor in cardiac development: it regulates SMYD1 (which activates HAND2) and KDR (which with HAND2 orchestrates outflow tract formation). GATA6 loss-of-function variants perturb cardiac and endoderm lineage genes directing PDX1/pancreatic development. An exon 4 GATA6 missense variant causes ectopic pioneer activities, reducing GATA4, FOXA1/2, and PDX1 and increasing retinoic acid signaling promoting diaphragm development. |
Isogenic iPSC cardiomyocyte differentiation, RNA-seq, ATAC-seq (chromatin accessibility), ChIP-seq, GATA6 LoF and missense variant comparison |
eLife |
High |
33054971
|
| 2020 |
EZH2 transcriptionally represses GATA6 in PDAC via H3K27 methylation; genetic or pharmacologic EZH2 depletion increases GATA6 expression and induces a classical gene signature, while GATA6 re-ablation in EZH2-deficient cells rescues invasive capacity and basal gene signature. |
ChIP-seq (EZH2 on GATA6 locus), RNA-seq, GATA6 knockdown in EZH2-depleted cells, transgenic PDAC models |
Cancer research |
High |
32907838
|
| 2020 |
GATA6 directly binds the promoter of VEGF-C at its promoter region and acts as a transcriptional repressor; loss of GATA6 in bladder cancer (via promoter hypermethylation) leads to VEGF-C upregulation, promoting lymphangiogenesis and lymph node metastasis. |
ChIP assay, promoter binding assay, GATA6 reconstitution and knockdown, in vivo lymph node metastasis model |
FASEB journal |
Medium |
32103545
|
| 2020 |
GATA6 directly upregulates MUC1 expression by binding to GATA-motifs at positions -1584 and -1456 in the MUC1 promoter; MUC1 then binds to β-catenin and increases nuclear β-catenin levels, driving EMT and metastasis in cholangiocarcinoma. |
ChIP-seq, luciferase reporter assay with point-mutant GATA sites, co-immunoprecipitation (MUC1/β-catenin), knockdown/overexpression, in vivo metastasis |
Cell death & disease |
Medium |
33060563
|
| 2020 |
GATA6 controls insulin biosynthesis/secretion in adult β-cells and lung specification from human PSCs: knockdown of GATA6 during endoderm patterning increases NKX2.1+ lung progenitors, while GATA6 ablation impairs terminal lung differentiation; transgenic GATA6 expression skews development toward liver fate at the expense of lung progenitors, revealing a dosage effect. |
GATA6 knockdown and null hPSC lines, directed differentiation to lung progenitors, flow cytometry, gene expression analysis |
The Journal of clinical investigation |
Medium |
29889101
|
| 2020 |
TET2 marks the GATA6 locus with 5-hydroxymethylcytosine (5hmc) to maintain classical PDAC phenotype; SMAD4 directly supports TET2 levels, and loss of SMAD4 reduces 5hmc, GATA6 expression, and promotes squamous-like tumors. Restoring TET2 stability with metformin/vitamin C restores 5hmc and GATA6 levels and reverts squamous-like phenotype in vitro and in vivo. |
Oxidative bisulfite sequencing (genome-wide 5hmc and 5mc mapping), in vivo pharmacological rescue, bioinformatics iCluster |
Gastroenterology |
Medium |
33915173
|
| 2021 |
HDAC1/2 suppress GATA6 expression by promoting STAT3 acetylation, which enhances DNMT1 binding to STAT3 and leads to hypermethylation of the GATA6 promoter CpG region (+140/+255); blocking STAT3 acetylation at Lys685 disrupts DNMT1-STAT3 interaction and reverses GATA6 promoter methylation, demonstrating an epigenetic regulatory mechanism for GATA6 in endothelial cells. |
Romidepsin treatment, HDAC1/2 siRNA, methylation-specific PCR, ChIP (STAT3 enrichment at GATA6 promoter), STAT3 Lys685Arg mutation, Co-IP (DNMT1-STAT3), in vivo atherosclerosis model |
Theranostics |
Medium |
33859766
|
| 2021 |
A GATA6-centered gene regulatory network involving HNF1A and HNF4A controls PDAC subtype identity; GATA6 loss alone is necessary but not sufficient for basal program expression—concomitant loss of HNF1A and HNF4A (through epigenetic silencing) is required for the full phenotype switch. In mice, late Gata6 deletion dramatically increased metastatic rate. |
Dual-recombinase mouse model (Gata6LateKO), RNA-seq of primary tumor cells, human transcriptomics datasets, tissue samples |
Gut |
High |
33846140
|
| 2021 |
GATA6 directly activates TBX3 and EDN1 as key regulators of the sinus node genetic program (in conduction and non-conduction cells, respectively); Gata6 haploinsufficiency causes hypoplastic sinus node and rhythm abnormalities, and cell-specific deletion reveals requirements in multiple SAN lineages. |
Gata6 heterozygous and cell-specific conditional KO mice, ECG recording, histology, chromatin binding and transcriptional activation assays |
Proceedings of the National Academy of Sciences of the United States of America |
High |
33443158
|
| 2022 |
GATA6 and NANOG co-bind at the vast majority of epiblast and PrE enhancers both in embryonic stem cells and in blastocysts; upon GATA6 induction, co-binding is followed by eviction of Epi TFs, rapid chromatin remodeling and remodeling of enhancer-promoter contacts to establish PrE lineage while repressing Epi fate. |
Inducible GATA6 in ES cells, ChIP-seq (GATA6 and NANOG), ATAC-seq, Hi-C/4C (enhancer-promoter contacts), blastocyst ChIP |
Nature communications |
High |
35871075
|
| 2022 |
EP300 (p300) histone acetyltransferase directly supports GATA6 expression; loss of EP300 downregulates GATA6 and silences the GATA6-regulated differentiation program, causing a phenotypic switch from classical to basal-like/squamous PDAC subtype and resistance to PORCN (Wnt) inhibitors. |
In vivo CRISPR screen, EP300 knockdown/KO, GATA6 overexpression rescue, RNA-seq, chromatin accessibility mapping |
The Journal of clinical investigation |
High |
35536676
|
| 2022 |
Endothelial Gata6 deletion reduces atherosclerosis by decreasing monocyte infiltration and pro-inflammatory macrophage formation; Cmpk2 and Ccl5 are identified as direct target genes of GATA6 in endothelial cells mediating these effects through the CMPK2-Nlrp3 pathway. |
EC-specific Gata6 KO in ApoeKO mice, endothelial AAV9-Cmpk2-shRNA delivery, ChIP (direct target identification), monocyte adhesion and migration assays, lesion quantification |
Redox biology |
Medium |
37339559
|
| 2023 |
Gata6 deletion from the brown fat lineage causes a striking loss of brown adipose tissue, identifying GATA6 as a crucial regulator of brown adipocyte development; GATA6 marks brown adipogenic progenitor cells. |
Single-cell gene expression analysis, immunostaining, lineage tracing, conditional Gata6 KO in brown fat lineage |
Developmental cell |
Medium |
37647897
|
| 2023 |
SIRT6 inhibits GATA6 transcription by deacetylating and increasing degradation of the transcription factor Nkx2.5 (which would otherwise activate GATA6); GATA6 in turn impedes ATM-mediated DNA damage repair, leading to accelerated VSMC senescence and osteogenic differentiation. Gata6 knockdown (via AAV-shRNA) inhibits arterial calcification in CKD mice. |
SIRT6-transgenic mice, Gata6 AAV-shRNA knockdown, in vitro gain/loss-of-function, co-immunoprecipitation (SIRT6-Nkx2.5), DNA damage repair assays (ATM pathway) |
Kidney international |
Medium |
37914087
|
| 2012 |
GATA-6 and NF-κB bind to specific sites on the CPI-17 promoter and upregulate CPI-17 expression in an additive manner in bladder smooth muscle cells; CPI-17 inhibits myosin light chain phosphatase, thereby regulating Ca2+ sensitization and contractile force maintenance in smooth muscle. |
Promoter binding assays, EMSA, GATA-6 siRNA knockdown, NF-κB KO mice, smooth muscle force measurement |
Molecular and cellular biology |
Medium |
23275439
|
| 2016 |
Gain-of-function GATA6 variants (R585L, P91S, A177T) show markedly upregulated transcriptional activity in reporter assays and enhanced activation of ANP and alpha-MHC promoters when co-expressed with GATA4 and MEF2C, demonstrating that gain-of-function GATA6 mutations can drive atrial fibrillation. |
Whole exome sequencing, luciferase reporter assay with wild-type and mutant GATA6 constructs, co-expression with GATA4/MEF2C |
Heart rhythm |
Medium |
27756709
|
| 2015 |
REG4 is a direct transcriptional target of GATA6; GATA6-mediated activation of REG4 enhances adherent growth of colon cancer cells, while LGR5 activation by GATA6 drives clonogenicity, with both being suppressed by miR-363 targeting of GATA6. |
GATA6 overexpression/knockdown, miR-363 overexpression, gene expression analysis, colon cancer cell proliferation/tumorigenicity assays |
Scientific reports |
Medium |
26387746
|