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Coordinating Tissue Regeneration through TGF-β Activated Kinase 1 (TAK1) In-activation and Re-activation

ABSTRACT: Coordinating Tissue Regeneration through TGF-β Activated Kinase 1 (TAK1) In-activation and Re-activation

PROVIDER: PRJNA521049 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8534342_1.fastq.gz	Fastqsanger.gz
	SRR8534342_2.fastq.gz	Fastqsanger.gz
	SRR8534343_1.fastq.gz	Fastqsanger.gz
	SRR8534343_2.fastq.gz	Fastqsanger.gz
	SRR8534344_1.fastq.gz	Fastqsanger.gz

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Coordinating Tissue Regeneration through TGF-β Activated Kinase 1 (TAK1) In-activation and Re-activation

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Expression profiling in palatal mesenchymal cells stimulated with TGF-beta2 in the presence and absence of TGFbRI and Tak1 kinase inhibitors

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Project description:The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-?B subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-?B p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-?B-dependent enhancers in epithelial cells. RNA-seq of KB cells either untreated or treated with IL-1 alpha

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