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Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer [ChIP-Seq]

ABSTRACT: To identifiy core GATA6 functions and transcriptional targets in human gastric cancer, including additional subservient transcriptional regulators via integrative analysis of GATA6 transcription factor occupancy, gene dependency, and tumor synexpression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE51936 | GEO | 2013/12/02

SECONDARY ACCESSION(S): PRJNA225860

REPOSITORIES: GEO

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Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer (microarray)

Project description:To identifiy core GATA6 functions and transcriptional targets in human gastric cancer, including additional subservient transcriptional regulators via integrative analysis of GATA6 transcription factor occupancy, gene dependency, and tumor synexpression.

2013-12-02 | GSE43196 | GEO

Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer [ChIP-Seq]

2013-12-02 | E-GEOD-51936 | biostudies-arrayexpress

Genome-wide analyses of GATA6 occupancy and functions provide insights into its oncogenic mechanisms in human gastric cancer (microarray)

2013-12-02 | E-GEOD-43196 | biostudies-arrayexpress

GATA6-AS1 Regulates GATA6 Expression to Modulate Human Endoderm Differentiation

Project description:Transcriptome analysis has uncovered a series of long noncoding RNAs (lncRNAs) transcribed during cell differentiation. Here, we uncovered lncRNA GATA6-AS1 is a functional lncRNA in definitive endoderm (DE) differentiation. We found GATA6-AS1 positively regulated the expression of endoderm key factor GATA6, which was different from previous reports in other biological contexts. Further investigation showed GATA6-AS1 interacted with SMAD2/3 and recruited SMAD2/3 to the promoter region of the GATA6 gene locus. In addition, overexpression of GATA6 was able to rescue the defect of DE differentiation due to the absence of GATA6-AS1, suggesting GATA6 was the functional target of GATA6-AS1 during endoderm differentiation. Ultimately, our study uncovers GATA6-AS1 is necessary for DE and pancreas differentiation, and reveals the detailed regulation mechanism between GATA6-AS1 and DE differentiation.

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Gene expression signature of Gata6 positive epidermal cells.

2017-05-16 | GSE62606 | GEO

Expression profile of GATA6 deficient pancreatic islets

Project description:GATA6 mutations have been linked to adult-onset diabetes with subclinical or no exocrine insufficiency suggesting an important role for GATA6 in humanβcell physiology. To investigate the role of GATA6 in adult endocrine pancreas, we generated mice in which Gata6 is specifically inactivated in the pancreas. These mice develop glucose intolerance. Islets deficient in GATA6 activity display decreased insulin content and impaired glucose-induced insulin secretion. Gata6-deficient ß cells exhibit ultrastructural abnormalities including increased immature insulin granules, swollen mitochondria and disorganized endoplasmic reticulum. Microarray analysis revealed that loss of GATA6 greatly impacts ß cell specific gene expression.

2019-10-31 | GSE106316 | GEO

Gene expression signature of Gata6 positive epidermal cells.

Project description:To characterize gene expression in Gata6 positive epidermal cells we analyzed a Gata6 reporter mouse in which the endogenous Gata6 promoter drives expression of mTomato. We performed flow cytometry followed by transcriptome analysis. We compared four subpopulations of telogen epidermal cells: Gata6+/Itga6+ cells, Gata6+/itga6- cells, CD34+/Itga6+ cells (which are Gata6-) and all remaining Itga6+ cells (Gata6-/CD34-). The RNA was isolated from age and sex matched mice. We compared four subpopulations of telogen epidermal cells: Gata6+/Itga6+ cells, Gata6+/itga6- cells, CD34+/Itga6+ cells (which are Gata6-) and all remaining Itga6+ cells (Gata6-/CD34-). The RNA was isolated from age and sex matched mice. Three biological replicates for each cell population were analyzed

2017-05-16 | E-GEOD-62606 | biostudies-arrayexpress

GATA6 dependent gene regulation in peritoneal macrophages

Project description:Peritoneal macrophages from control and Mac-Gata6 KO (LysM-cre;Gata6-floxed) mice were determined for genome wide gene expression.

2014-05-02 | GSE56684 | GEO

GATA6 dependent gene regulation in peritoneal macrophages

Project description:Peritoneal macrophages from control and Mac-Gata6 KO (LysM-cre;Gata6-floxed) mice were determined for genome wide gene expression. Sorted peritoneal macrophages from control and Mac-Gata6 KO mice were performed for whole genome expression analysis by Illumina microarray

2014-05-02 | E-GEOD-56684 | biostudies-arrayexpress

Genes regulated by GATA6 in the lung

Project description:Epithelial organs including the lung are known to possess regenerative abilities through activation of endogenous stem cell populations but the molecular pathways regulating stem cell expansion and regeneration are not well understood. Here we show that Gata6 regulates the temporal appearance and number of bronchioalveolar stem cells (BASCs) in the lung leading to the precocious appearance of BASCs and concurrent loss in epithelial differentiation in Gata6 null lung epithelium. This expansion of BASCs is the result of a dramatic increase in canonical Wnt signaling in lung epithelium upon loss of Gata6. Expression of the non-canonical Wnt receptor Fzd2 is down-regulated in Gata6 mutants and increased Fzd2 or decreased β-catenin expression rescues, in part, the lung epithelial defects in Gata6 mutants. During lung epithelial regeneration, we show that canonical Wnt signaling is activated in the niche containing BASCs and forced activation of Wnt signaling leads to a dramatic increase in BASC numbers. Moreover, Gata6 is required for proper lung epithelial regeneration and postnatal loss of Gata6 leads to increased BASC expansion and decreased differentiation. Together, these data demonstrate that Gata6 regulated Wnt signaling controls the balance between stem/progenitor expansion and epithelial differentiation required for both lung development and regeneration. Keywords: gene targets in knockout mouse model

2008-04-15 | GSE11165 | GEO

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