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IER5 is required for Notch-mediated induction of squamous cell differentiation [H3K27ac ChIP-seq]

ABSTRACT: IER5 is required for Notch-mediated induction of squamous cell differentiation [H3K27ac ChIP-seq]

PROVIDER: PRJNA658110 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12477024.fastq.gz	Fastqsanger.gz
	SRR12477025.fastq.gz	Fastqsanger.gz
	SRR12477026.fastq.gz	Fastqsanger.gz
	SRR12477027.fastq.gz	Fastqsanger.gz
	SRR12477028.fastq.gz	Fastqsanger.gz

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IER5 is required for Notch-mediated induction of squamous cell differentiation [H3K27ac ChIP-seq]

Project description:Conditional activation of Notch in squamous cells activates a context-specific gene expression program through lineage-specific regulatory elements. IER5 is a direct Notch-regulated gene and required for Notch-induced differentiation of squamous carcinoma cells.

2020-08-31 | GSE156485 | GEO

IER5 is required for Notch-mediated induction of squamous cell differentiation [RNA-seq]

2020-08-31 | GSE156487 | GEO

IER5 is required for Notch-mediated induction of squamous cell differentiation [ChIP-seq RBPJ & MAML1]

2020-08-31 | GSE156486 | GEO

IER5 is required for Notch-mediated induction of squamous cell differentiation

Project description:IER5 is required for Notch-mediated induction of squamous cell differentiation

| PRJNA658108 | ENA

IER5 is required for Notch-mediated induction of squamous cell differentiation [RNA-seq]

Project description:IER5 is required for Notch-mediated induction of squamous cell differentiation [RNA-seq]

| PRJNA658112 | ENA

IER5 is required for Notch-mediated induction of squamous cell differentiation [ChIP-seq RBPJ & MAML1]

Project description:IER5 is required for Notch-mediated induction of squamous cell differentiation [ChIP-seq RBPJ & MAML1]

| PRJNA658109 | ENA

IER5 is a novel Notch target gene that contributes to the effects of Notch on breast cancer stem / progenitor cells

Project description:The Notch signalling pathway has been implicated in the development and progression of numerous malignancies, including breast cancer. In breast cancer, the transcriptional programs elicited by Notch activation and the target genes responsible for mediating the downstream effects of the pathway remain poorly understood. Here, we characterise the immediate cellular consequences of Notch activation in breast cancer cells and identify a panel of direct Notch targets with potential relevance in the disease. One key direct transcriptional target of Notch in this context is IER5. Functionally, IER5 activation in breast cancer contributes to the effects of Notch signalling on the self-renewal and proliferative potential of breast cancer stem and progenitor cells. High levels of IER5 mRNA may be an important biomarker indicative of Notch activation in the disease.

2018-01-08 | GSE30288 | GEO

Induction of osteogenesis by bone-targeted Notch activation

Project description:Induction of osteogenesis by bone-targeted Notch activation

| PRJNA638902 | ENA

ChIP-seq of H3K27ac in lung cancer, endometrial carcinoma and head and neck squamous cell carcinoma cells.

Project description:Using H3K27ac ChIP-seq profile to map active enhancers in lung cancer, endometrial carcinoma and head and neck squamous cell carcinoma cells

2015-10-26 | GSE66992 | GEO

Notch signaling is required for induction of an innate T cell development program in human thymus

Project description:CD4 CD8 double positive (DP) thymocytes progressively shut down Notch signaling after β-selection allowing progression of the DP program and positive selection of conventional CD4 and CD8 single positive T cells. In contrast, innate CD8+ T cells are selected from DP precursors shortly after β-selection. Here, we investigated whether notch signaling is required for the initiation of the innate T cell developmental program upon TCR engagement. We show that, after β-selection, Notch activation limits progression to late DP cells and favors the development of TCRαβ/CD3 expressing CD8dim early DP progenitors. TCR engagement in these Notch dependent TCRαβ+ early DP precursors does not induce prominent apoptosis, but rather induces T-bet expression by an mTOR-dependent mechanism. Our findings indicate that Notch signaling drives the launch of an innate effector program in response to TCR agonist selection in the thymus.

2019-09-05 | GSE100519 | GEO

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