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MYB ChIP-Seq of K562 cells

ABSTRACT: MYB ChIP-Seq of K562 cells

PROVIDER: PRJNA512464 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8383000.fastq.gz	Fastqsanger.gz
	SRR8383001.fastq.gz	Fastqsanger.gz
	SRR8383002.fastq.gz	Fastqsanger.gz
	SRR8383003.fastq.gz	Fastqsanger.gz
	SRR8382994.fastq.gz	Fastqsanger.gz

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MYB ChIP-Seq of K562 cells

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Bidirectional enhancer RNAs regulate different MYB promoters

Project description:MYB is a pivotal oncogenic driver in leukemia and is overexpressed through various mechanisms. Transcriptional regulation of MYB is complex with an alternative MYB promoter (TSS2) located in intron 1. Here, we identified two bidirectional enhancer RNAs transcribed from the -34 kb enhancer of MYB. These two eRNAs both upregulate MYB transcription, and promote proliferation and migration in leukemia cells. To further elucidate how eRNAs regulate MYB expression, we analyzed MYB differential exon usage in RNASeq data with the DEXSeq package after overexpression of eRNAs in K562 cells. We found that bidirectional enhancer RNAs regulate different MYB promoters. Transcription initiating from TSS2 produces N-terminally truncated MYB protein lacking the first 20 amino acids. To analyze the genes and pathways affected by both MYB isoforms, RNA-seq was performed after MYB or N-terminally truncated MYB was overexpressed in K562 cells. We found that N-terminally truncated MYB exhibits different activity in K562 cells, where it not only activates different primary targets, but also different downstream pathways altogether.

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ChIP-seq analysis of dCas9 chromatin occupancy in K562 cells by CAPTURE2.0

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2019-03-21 | PXD012930 | Pride

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