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Determination of Shavenbaby target genes in early Enterocytes (eECs)

ABSTRACT: Determination of Shavenbaby target genes in early Enterocytes (eECs)

PROVIDER: PRJNA910223 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22578426.fastq.gz	Fastqsanger.gz
	SRR22578427.fastq.gz	Fastqsanger.gz
	SRR22578428.fastq.gz	Fastqsanger.gz
	SRR22578429.fastq.gz	Fastqsanger.gz
	SRR22578430.fastq.gz	Fastqsanger.gz

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Determination of Shavenbaby target genes in early Enterocytes (eECs)

Project description:Shavenbaby (Svb) transcription factor is involved in the homeostasis of intestinal stem cells (ISCs), and the differentiation of their enteroblast progeny (EB) into enterocytes (EC). Svb is produced as a long repressor protein called SvbRepressor (SvbREP). In presence of Pri peptides SvbREP is processed into a shorter activator form (SvbACT) through partial proteasomal degradation of the REP domain. In ISCs/EBs, Pri triggers SvbREP to ACT maturation, while SvbREP form accumulates in differentiated enterocytes. The absence of Svb promote the apoptosis of the intestinal stem cells. In ISCs/EBs, the ectopic expression of SvbREP form promotes the differentiation and the overexpression of SvbACT promotes hyperplasia. (Al Hayek, et al 2020) Based on these functional analyses, Svb appears to control ISC/EB survival and behavior, balancing proliferation and differentiation through a molecular switch between its 2 antagonistic isoforms. In this study, we determine the Svb target genes in different cell types along the intestinal cell lineage. This particular metadata sheet refers to early enterocytes (eEC) transcriptomic data (RNAseq) in control condition and upon modulation of Svb function.

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Project description:Shavenbaby (Svb) transcription factor is involved in the homeostasis of intestinal stem cells (ISCs), and the differentiation of their enteroblast progeny (EB) into enterocytes (EC). Svb is produced as a long repressor protein called SvbRepressor (SvbREP). In presence of Pri peptides SvbREP is processed into a shorter activator form (SvbACT) through partial proteasomal degradation of the REP domain. In ISCs/EBs, Pri triggers SvbREP to ACT maturation, while SvbREP form accumulates in differentiated enterocytes. The absence of Svb promote the apoptosis of the intestinal stem cells. In ISCs/EBs, the ectopic expression of SvbREP form promotes the differentiation and the overexpression of SvbACT promotes hyperplasia. (Al Hayek, et al 2020) Based on these functional analyses, Svb appears to control ISC/EB survival and behavior, balancing proliferation and differentiation through a molecular switch between its 2 antagonistic isoforms. In this study, we determine the Svb target genes in different cell types along the intestinal cell lineage. This particular metadata sheet refers to early enterocytes (mEC) transcriptomic data (RNAseq) in control condition and upon modulation of Svb function.

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Project description:Shavenbaby (Svb) transcription factor is involved in the homeostasis of intestinal stem cells (ISCs), and the differentiation of their enteroblast progeny (EB) into enterocytes (EC). Svb is produced as a long repressor protein called SvbRepressor (SvbREP). In presence of Pri peptides SvbREP is processed into a shorter activator form (SvbACT) through partial proteasomal degradation of the REP domain. In ISCs/EBs, Pri triggers SvbREP to ACT maturation, while SvbREP form accumulates in differentiated enterocytes. The absence of Svb promote the apoptosis of the intestinal stem cells. In ISCs/EBs, the ectopic expression of SvbREP form promotes the differentiation and the overexpression of SvbACT promotes hyperplasia. (Al Hayek, et al 2020) Based on these functional analyses, Svb appears to control ISC/EB survival and behavior, balancing proliferation and differentiation through a molecular switch between its 2 antagonistic isoforms. In this study, we determine the Svb target genes in different cell types along the intestinal cell lineage. This particular metadata sheet refers to enteroblast (EB) transcriptomic data (RNAseq) in control condition and upon modulation of Svb function.

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