Genomics

Dataset Information

42

Disease Model of GATA4 Mutation Reveals Transcription Factor Cooperativity in Human Cardiogenesis [ChIP-Seq]


ABSTRACT: Heterozygous mutations in GATA4 cause congenital heart defects and cardiomyopathy through unknown mechanisms. To gain insights into the genome-wide localization perturbations during human cardiac development due to GATA4 heterozygosity, we performed ChIP-seq of wildtype and GATA4-G296S diseased cardiomyocytes. Overall design: ChIP sequencing of GATA4, TBX5, MED1, H3K4me3, H3K36me3, H3K27ac, H3K27me3, plus input, from 75 wildtype or diseased pluripotent stem cell derived cardiomyocytes

INSTRUMENT(S): Illumina HiSeq 2000 (Homo sapiens)

SUBMITTER: Yen-Sin Ang 

PROVIDER: GSE85628 | GEO | 2016-12-15

SECONDARY ACCESSION(S): PRJNA339028

REPOSITORIES: GEO

Dataset's files

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Publications


Mutation of highly conserved residues in transcription factors may affect protein-protein or protein-DNA interactions, leading to gene network dysregulation and human disease. Human mutations in GATA4, a cardiogenic transcription factor, cause cardiac septal defects and cardiomyopathy. Here, iPS-derived cardiomyocytes from subjects with a heterozygous GATA4-G296S missense mutation showed impaired contractility, calcium handling, and metabolic activity. In human cardiomyocytes, GATA4 broadly co-o  ...[more]

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