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KLF3 mediates epidermal differentiation through the epigenomic writer CBP [RNA-seq]

ABSTRACT: KLF3 mediates epidermal differentiation through the epigenomic writer CBP [RNA-seq]

PROVIDER: PRJNA591620 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10530013.fastq.gz	Fastqsanger.gz
	SRR10530014.fastq.gz	Fastqsanger.gz
	SRR10530015.fastq.gz	Fastqsanger.gz
	SRR10530016.fastq.gz	Fastqsanger.gz
	SRR10530017.fastq.gz	Fastqsanger.gz

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KLF3 mediates epidermal differentiation through the epigenomic writer CBP

Project description:KLF3 mediates epidermal differentiation through the epigenomic writer CBP

| PRJNA596256 | ENA

KLF3 mediates epidermal differentiation through the epigenomic writer CBP [ChIP-seq]

Project description:The differentiated layers of the epidermis protect the body from the outside environment. Impairments in the differentiation process can lead to skin diseases that can afflict ~20% of the population. Thus, it is of utmost importance to characterize and understand the factors that promote the differentiation process. Here we identify the transcription factor KLF3 as a novel regulator of epidermal differentiation. Knockdown of KLF3 results in reduced differentiation gene expression and increased cell cycle gene expression. Over 50% of KLF3’s genomic binding sites occur at regions containing H3K4me/H3K27ac with the vast majority at active enhancers. KLF3 bound to active enhancers proximal to differentiation genes that are dependent upon KLF3 for expression. Based on this association, we sought to investigate KLF3’s possible relationship with the enhancer associated proteins CBP and P300. Analysis of the transcriptome controlled by CBP and P300 showed that CBP and KLF3 control a similar gene expression program and are both essential for promoting differentiation. In addition, 35% of CBP’s genomic binding sites overlap with KLF3 and knockdown of KLF3 results in reduced CBP localization at enhancers proximal to differentiation gene clusters. Our results suggest that KLF3 regulates differentiation gene expression by promoting CBP localization at enhancers.

2020-07-22 | GSE140991 | GEO

KLF3 mediates epidermal differentiation through the epigenomic writer CBP [RNA-seq]

2020-07-22 | GSE140990 | GEO

KLF3 mediates epidermal differentiation through the epigenomic writer CBP [ChIP-seq]

Project description:KLF3 mediates epidermal differentiation through the epigenomic writer CBP [ChIP-seq]

| PRJNA591622 | ENA

KLF3 Mediates Epidermal Differentiation through the Epigenomic Writer CBP.

Project description:Impairments in the differentiation process can lead to skin diseases that can afflict ∼20% of the population. Thus, it is of utmost importance to understand the factors that promote the differentiation process. Here we identify the transcription factor KLF3 as a regulator of epidermal differentiation. Knockdown of KLF3 results in reduced differentiation gene expression and increased cell cycle gene expression. Over half of KLF3's genomic binding sites occur at active enhancers. KLF3 binds to active enhancers proximal to differentiation genes that are dependent upon KLF3 for expression. KLF3's genomic binding sites also highly overlaps with CBP, a histone acetyltransferase necessary for activating enhancers. Depletion of KLF3 causes reduced CBP localization at enhancers proximal to differentiation gene clusters, which leads to loss of enhancer activation but not priming. Our results suggest that KLF3 is necessary to recruit CBP to activate enhancers and drive epidermal differentiation gene expression.

| S-EPMC7358749 | biostudies-literature

KLF3 mediates epidermal differentiation through the epigenomic writer CBP

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-07-22 | GSE142225 | GEO

Microarray analysis of wildtype, Klf3 H275R homozygous and heterozygous, Klf3 CH gene trap homozygous and heterozygous E12.5 embryos

2013-01-31 | GSE43908 | GEO

Microarray analysis of wildtype, Klf3 H275R homozygous and heterozygous, Klf3 CH gene trap homozygous and heterozygous E12.5 embryos

Project description:The aim of this experiment was to investigate the dysregulation of gene expression in whole E12.5 embryos containing a gene trap (CH) or point mutation (H275R) within the Klf3 gene Affymetrix microarrays were performed on RNA from wildtype, Klf3 H275R/H275R, Klf3 H275R/+, Klf3 CH homozygous and Klf3 CH heterozygous E12.5 embryos Four wildtype replicates, three Klf3 H275R/H275R replicates, four Klf3 H275R/+ replicates, four Klf3 CH homozygous replicates and two Klf3 CH heterozygous replicates of whole E12.5 embryos, litter-matched where possible.

2013-01-31 | E-GEOD-43908 | biostudies-arrayexpress

Microarray analysis of wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt TER119+ E13.5 fetal liver cells

2013-01-17 | GSE43524 | GEO

Microarray analysis of wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt TER119+ E13.5 fetal liver cells

Project description:The aim of this experiment was to investigate the regulation of gene expression by KLF3 and KLF8 in fetal erythroid cells by analyzing single and double mutant mouse models. Affymetrix microarrays were performed on RNA from TER119+ fetal liver cells from E13.5 wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt mice. Four wildtype replicates, four Klf8gt/gt replicates, three Klf3-/- replicates and four Klf3-/- Klf8gt/gt replicates of E13.5 TER119+ fetal liver cell samples, litter-matched where possible.

2013-01-17 | E-GEOD-43524 | biostudies-arrayexpress

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