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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (DSS)

ABSTRACT: TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (DSS)

PROVIDER: PRJNA848222 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19631292_1.fastq.gz	Fastqsanger.gz
	SRR19631292_2.fastq.gz	Fastqsanger.gz
	SRR19631293_1.fastq.gz	Fastqsanger.gz
	SRR19631293_2.fastq.gz	Fastqsanger.gz
	SRR19631294_1.fastq.gz	Fastqsanger.gz

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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (DSS)

Project description:TO highlight an integral role of the TGF-β/Smad4 axis in restraining intestinal inflammation and suggest TGF-β or Yap signaling as potential therapeutic targets in inflammatory bowel disease patients with decreased Smad4 expression. We then performed gene expression profiling analysis using data obtained from RNA-seq of colonic epithelia cells derived from DSS treatment.

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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (organoids)

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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner

Project description:TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner

| PRJNA848220 | ENA

TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (organoids)

Project description:TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner (organoids)

| PRJNA848221 | ENA

Gene expression profile of ATF6a and ATF6b knockout mice with dextran sulfate sodium (DSS)-induced colitis

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TGF-β promotes colitis and cancer development in Smad4-deficient intestinal epithelium in a Yap-dependent manner

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

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Loss of SETD2 aggravates colorectal cancer progression caused by SMAD4 deletion through the RAS/MAPK pathway [RNA-seq]

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