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Smad3 binding regions in differentiated human progenitor epidermal keratinocytes (HPEK).

ABSTRACT: Smad3 binding regions in differentiated human progenitor epidermal keratinocytes (HPEK).

PROVIDER: PRJNA747268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15175846.fastq.gz	Fastqsanger.gz
	SRR15175847.fastq.gz	Fastqsanger.gz

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Smad3 binding regions in human epidermal keratinocytes (HaCaT).

Project description:Smad3 binding regions in human epidermal keratinocytes (HaCaT).

| PRJNA782488 | ENA

Smad3 binding regions in differentiated human progenitor epidermal keratinocytes (HPEK).

Project description:Smad family proteins transduce signals downstream of transforming growth factor-beta (TGF-beta) and are one of the factors that regulate target genes related to diseases affecting the skin. We here identified C2orf54, officially known as MAB21L4, as one of the most up-regulated targets of TGF-beta and Smad3 in a differentiated human progenitor epidermal keratinocyte, using chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq). Smad2 and Smad3 bind to the regulatory regions of the C2orf54 gene locus. We found that TGF-beta induced expression of a barrier protein involucrin (encoded by IVL gene), and transcriptional activity of the IVL promoter induced by TGF-beta was inhibited by siRNAs for C2orf54. Further analysis revealed that C2orf54 siRNAs also down-regulated the expression of several target genes of TGF-beta. C2orf54 protein located mainly in the cytosol, physically bound to Smad2 and Smad3, but did not inhibit the binding of Smad2 and Smad3 to the target genomic regions. These findings suggested that TGF-beta-induced C2orf54 up-regulates gene expression induced by Smads, possibly through its physical interaction with Smad proteins.

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Smad3 binding regions in human epidermal keratinocytes (HaCaT).

Project description:Smad proteins transduce signals downstream of transforming growth factor-b (TGF-b), and are one of the factors that regulate the expression of genes related to diseases affecting the skin. In the present study, we identified MAB21L4, also known as male abnormal 21 like 4 or C2orf54, as one of the most up-regulated targets of TGF-b and Smad3 in differentiated human progenitor epidermal keratinocytes using chromatin immunoprecipitation sequencing (ChIP-seq) and RNA sequencing (RNA-seq). Smad2 and Smad3 bound to the regulatory regions of the MAB21L4 gene locus. We found that TGF-b induced expression of the barrier protein involucrin (encoded by the IVL gene). Transcriptional activity of the IVL promoter induced by TGF-b was inhibited by siRNAs for MAB21L4. Further analysis revealed that MAB21L4 siRNAs also down-regulated the expression of several target genes of TGF-b. MAB21L4 protein was located mainly in the cytosol, where it was physically bound to Smad3 and a transcriptional corepressor c-Ski. siRNAs for MAB21L4 did not inhibit the binding of Smad3 to their target genomic regions but down-regulated acetylation of histone H3 lys 27 (H3K27ac), an active enhancer mark, near the Smad3 binding regions. These findings suggest that TGF-b-induced MAB21L4 up-regulates the gene expression induced by TGF-b, possibly through physical interactions with a transcriptional corepressor c-Ski in the cytosol.

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RNA-seq in human progenitor epidermal keratinocytes (HPEK) stimulated with TGF-beta.

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Expression data from epidermal human skin (stem cells, transient amplifying cells, differentiated cells)

Project description:Performing global gene expression profiling for different types of keratinocytes colonies can provide important information that might help in understanding the biology and ontogeny of epidermal skin stem cells. We used microarrays to detail the global gene expression profiling for different types of keratinocytes colonies including Holoclones (stem cells), Meroclones (transient amplifying cells), and Paraclones (differentiated cells) .

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Human epidermal keratinocytes treated with retinoic acid or thyroid hormone

Project description:Targets of Retinoic Acid (RA) were identified in primary human epidermal keratinocytes grown in the presence or absence of all-trans retinoic acid for 1, 4, 24, 48 and 72 hours. Targets of Thyroid Hormone (T3) were identified in primary human epidermal keratinocytes grown in the presence or absence of the hormone; same controls as for RA. Time course, 1, 4, 24, 48 and 72 hours

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