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Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ChIP-Seq]

ABSTRACT: Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ChIP-Seq]

PROVIDER: PRJNA495077 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7982850.fastq.gz	Fastqsanger.gz
	SRR7982860.fastq.gz	Fastqsanger.gz
	SRR7982851.fastq.gz	Fastqsanger.gz
	SRR7982861.fastq.gz	Fastqsanger.gz
	SRR7982852.fastq.gz	Fastqsanger.gz

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Similar Datasets

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program

Project description:Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program

| PRJNA495076 | ENA

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [RNA-Seq]

Project description:Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [RNA-Seq]

| PRJNA495078 | ENA

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ATAC-seq]

Project description:Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ATAC-seq]

| PRJNA533665 | ENA

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ATAC-seq]

Project description:In order to investigate whether Bcl11b mediates any chormatin accebility in Treg cell, we performed ATAC-Seq from Bcl11b sufficient (WT) and Bcl11b deficient Treg(KO) cells.We used 100,000 cells for each experiment.

2019-08-07 | GSE130059 | GEO

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [ChIP-Seq]

Project description:In order to identify Bcl11b-bound sites in Treg cells(WT) and Tn cells and to determine Bcl11n and Foxp3 peak overlaps, we performed Bcl11b and Foxp3 ChIP-seq on respective cell populations. In order to understand whether Bcl11b recruitment to it's target sites is dependent on Foxp3 we performed Bcl111b ChIP-Seq in Tfn cells(derived from Foxp3GFPKO mice). Finally, to ask whether genome-wide occupancy of Foxp3 is affected in the absence of Bcl11b, we performed Foxp3 ChIP-seq in Bcl11b-deficient Treg cells(KO Treg).

2019-08-07 | GSE120947 | GEO

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program [RNA-Seq]

Project description:In order to acquire in depth understanding of Treg specific molecular functions of Bcl11b, we performed RNA-Seq from Bcl11b-suffcient or deficient Treg cells to determine transcriptional profile.

2019-08-07 | GSE120946 | GEO

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of a regulatory T cell gene expression program.

Project description:Foxp3 and its protein partners establish a regulatory T (Treg) cell transcription profile and promote immunological tolerance. However, molecular features contributing to a Treg-specific gene expression program are still incompletely understood. We find that the transcription factor Bcl11b is a prominent Foxp3 cofactor with multifaceted functions in Treg biology. Optimal genomic recruitment of Foxp3 and Bcl11b is critically interdependent. Genome-wide occupancy studies coupled with gene expression profiling reveal that Bcl11b, in association with Foxp3, is primarily responsible in establishing a Treg-specific gene activation program. Furthermore, Bcl11b restricts misdirected recruitment of Foxp3 to sites, which would otherwise result in an altered Treg transcriptome profile. Consequently, Treg-specific ablation of Bcl11b results in marked breakdown of immune tolerance, leading to aggressive systemic autoimmunity. Our study provides previously underappreciated mechanistic insights into molecular events contributing to basic aspects of Treg function. Furthermore, it establishes a therapeutic target with potential implications in autoimmunity and cancer.

| S-EPMC6685721 | biostudies-literature

Bcl11b prevents catastrophic autoimmunity by controlling multiple aspects of regulatory T-cell gene expression program

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

2019-08-07 | GSE120948 | GEO

BCL11B

Project description:BCL11B

| PRJNA330816 | ENA

Genome-wide identification of Bcl11b gene targets

Project description:B-cell leukemia/lymphoma 11B (Bcl11b) is a transcription factor showing predominant expression in the striatum. To date, there are no known gene targets of Bcl11b in the nervous system. Here, we define targets for Bcl11b in striatal cells by performing genome-wide expression profiling. Transcriptome-wide analysis revealed that 694 genes were significantly altered in striatal cells over-expressing Bcl11b, including genes showing striatal-enriched expression similar to Bcl11b. Functional analysis on the gene target list identified significant association of Bcl11b to brain-derived neurotrophic factor/neurotrophin signaling. These data implicate Bcl11b as a novel regulator of the BDNF signaling pathway, which is disrupted in many neurological disorders. n=4 wt STHdh striatal cells and n=4 Bcl11b-transfected STHdh striatal cells

2011-08-01 | E-GEOD-31096 | biostudies-arrayexpress

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