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ChIP-seq data for H3K27 acetylation from 7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKβ

ABSTRACT: ChIP-seq data for H3K27 acetylation from 7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKβ

PROVIDER: PRJNA454903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7109576_1.fastq.gz	Fastqsanger.gz
	SRR7109576_2.fastq.gz	Fastqsanger.gz
	SRR7109577_1.fastq.gz	Fastqsanger.gz
	SRR7109577_2.fastq.gz	Fastqsanger.gz
	SRR7109578_1.fastq.gz	Fastqsanger.gz

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ChIP-seq data for H3K27 acetylation from 7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKβ

Project description:We found genetic deletion of IKKβ in mdx cardiomyocytes improved cardiac function and normalized calcium transients, and that differential gene expression favored a repressive function for NF-[kappa]B in these mice. We suspected that NF-[kappa]B was conferring a more restrictive chromatin conformation in a subset of genes. ChIP-seq was performed for H3K27 acetylation to show this repressive function for NF-[kappa]B was a global effect and to identify specific genes with more permissive chromatin conformation in hearts of mdx mice with IKKβ-deficient cardiomyocytes compared to mdx mice with intact IKKβ signaling.

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7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKβ

Project description:7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKβ

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Expression data from 7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKβ

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