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Characterization of the effect of deleting the Mib1 and Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

ABSTRACT: Characterization of the effect of deleting the Mib1 and Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

PROVIDER: PRJNA1101518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28724061.fastq.gz	Fastqsanger.gz
	SRR28724062.fastq.gz	Fastqsanger.gz
	SRR28724063.fastq.gz	Fastqsanger.gz
	SRR28724064.fastq.gz	Fastqsanger.gz
	SRR28724065.fastq.gz	Fastqsanger.gz

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Characterization of the effect of deleting the Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:Characterization of the effect of deleting the Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

| PRJNA1074230 | ENA

ChIP-seq for Gata6 and histone H3K27Ac on mouse branchial arches at E11.5.

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Characterization of the effect of deleting the Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:To investigate the role of Gata6 in OFT development, we generated a Gata6 heterozygous mice, harvested OFT at E11.5, and determined gene expression profiles, using bulk RNA-seq.

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Characterization of the effect of deleting the Mib1 and Gata6 gene in E (embryonic day) 11.5 OFT (outflow tract).

Project description:To investigate the potential interactions between of Gata6 and Mib1 in OFT development, we generated a double heterozygous mice Mib1V943F/+ Gata6STOP/+, harvested OFT at E11.5, and determined gene expression profiles, using RNA-seq.

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Project description:Neural crest defects lead to congenital heart disease involving outflow tract (OFT) malformation. Integrin-linked-Kinase (ILK) plays important roles in multiple cellular processes and embryogenesis. ILK is expressed in neural crest cells (NCC), but its role in NCC and OFT morphogenesis remains unknown. We used microarrays to detail the global programme of gene expression underlying the morphogenesis of the cardiac neural crest and outflow tract. The outflow tract of control and ILK mutant mouse embryos at E10.5 were dissected and dissociated. Neural crest cells were FACS sorted and used for RNA extraction and hybridization on Affymetrix microarrays.

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Project description:Gene expression profiling of the inferior and superior wall of the distal midgestation arterial domain (outflow tract) of the wild type CD1 mouse embryonic heart

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Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for PRDM6 in primary outflow tract smooth muscle cells overexpressing FLAG taggged PRDM6

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Deregulation of miRNAs in Infant Outflow Tract Myocardium of Non-syndromic Tetralogy of Fallot

Project description:Tetralogy of Fallot (TOF) is one of the most common heart defects in children and the underlying mechanisms remain elusive. miRNAs are a recently discovered class of regulators of gene expression and are becoming increasingly recognized as important regulators of heart development and function. The objective of the present study was to identify miRNAs that are abnormally expressed in clinical infant outflow tract myocardium tissues of TOFs. Microarray was used to analyze miRNA expression profiles in infant outflow tract myocardium tissues of TOFs and paired normal ones.

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Expression data from the neural crest cells isolated from mouse cardiac outflow tract at E10.5

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Project description:To identify a functional gene regulatory network that orchestrate transcriptional programs to direct proper outflow tract development, we generated transgenic mice harboring a 226bp-deletion within a GATA-dependent, highly conserved cardiac enhancer region. We then performed gene expression profiling analysis using data obtained from RNA-seq of outflow tract in wildtype and homozygous mutant littermates at embryonic day 12.5.

2023-10-04 | GSE227361 | GEO

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