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Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells.

ABSTRACT: Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells.

PROVIDER: PRJNA849644 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19665664_1.fastq.gz	Fastqsanger.gz
	SRR19665664_2.fastq.gz	Fastqsanger.gz
	SRR19665665_1.fastq.gz	Fastqsanger.gz
	SRR19665665_2.fastq.gz	Fastqsanger.gz
	SRR19665666_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [ChIP-seq]

Project description:Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [ChIP-seq]

| PRJNA849648 | ENA

Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [ATAC-seq]

Project description:Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [ATAC-seq]

| PRJNA849647 | ENA

Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [RNA-seq]

Project description:Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [RNA-seq]

| PRJNA849649 | ENA

Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [ChIP-seq]

Project description:Apoptosis is a genetically regulated program of cell death that plays a key role in immune disease processes. We identified EBF4, a little-studied member of the early B cell factor (EBF) family of transcription factors, in a whole-genome CRISPR screen for regulators of Fas/APO-1/CD95-mediated T cell death. Loss of EBF4 increases the half-life of the c-FLIP protein and its presence in the Fas signaling complex impairs caspase-8 cleavage and apoptosis. Transcriptome analysis revealed that EBF4 regulates molecules such as TBX21, EOMES, granzyme, and perforin that are important for human natural killer (NK) and CD8+ T cell functions Bio-ID - mass spectrometry analyses showed EBF4 binding to STAT3, STAT5, and MAP kinase 3, and a strong pathway relationship to IL-2 regulated genes which are known to govern cytotoxicity pathways ChIP-seq analysis defined a canonical EBF4 binding motif 5'-CCCNNGG/AG-3' closely related to the EBF1 binding site and using a luciferase-based reporter, we found a dose-dependent transcriptional response of this motif to EBF4. We also conducted ATAC-seq in EBF4 overexpressing cells and found increased chromatin accessibility upstream of granzyme and perforin and in topologically associated domains in human lymphocytes. Finally, we discovered that the EBF4 has basal expression in human but not mouse NK cells and CD8+ T cells and vanishes following activating stimulation. Together our data reveal key features of a previously unknown transcriptional regulator of human cytotoxic immune function.

2022-07-27 | GSE206219 | GEO

Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [RNA-seq]

Project description:Apoptosis is a genetically regulated program of cell death that plays a key role in immune disease processes. We identified EBF4, a little-studied member of the early B cell factor (EBF) family of transcription factors, in a whole-genome CRISPR screen for regulators of Fas/APO-1/CD95-mediated T cell death. Loss of EBF4 increases the half-life of the c-FLIP protein and its presence in the Fas signaling complex impairs caspase-8 cleavage and apoptosis. Transcriptome analysis revealed that EBF4 regulates molecules such as TBX21, EOMES, granzyme, and perforin that are important for human natural killer (NK) and CD8+ T cell functions. Bio-ID - mass spectrometry analyses showed EBF4 binding to STAT3, STAT5, and MAP kinase 3, and a strong pathway relationship to IL-2 regulated genes which are known to govern cytotoxicity pathways. ChIP-seq analysis defined a canonical EBF4 binding motif 5’-CCCNNGG/AG-3’ closely related to the EBF1 binding site and using a luciferase-based reporter, we found a dose-dependent transcriptional response of this motif to EBF4. We also conducted ATAC-seq in EBF4 overexpressing cells and found increased chromatin accessibility upstream of granzyme and perforin and in topologically associated domains in human lymphocytes. Finally, we discovered that the EBF4 has basal expression in human but not mouse NK cells and CD8+ T cells and vanishes following activating stimulation. Together our data reveal key features of a previously unknown transcriptional regulator of human cytotoxic immune function.

2022-07-27 | GSE206221 | GEO

Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells [ATAC-seq]

Project description:Apoptosis is a genetically regulated program of cell death that plays a key role in immune disease processes. We identified EBF4, a little-studied member of the early B cell factor (EBF) family of transcription factors, in a whole-genome CRISPR screen for regulators of Fas/APO-1/CD95-mediated T cell death. Loss of EBF4 increases the half-life of the c-FLIP protein and its presence in the Fas signaling complex impairs caspase-8 cleavage and apoptosis. Transcriptome analysis revealed that EBF4 regulates molecules such as TBX21, EOMES, granzyme, and perforin that are important for human natural killer (NK) and CD8+ T cell functions. Bio-ID - mass spectrometry analyses showed EBF4 binding to STAT3, STAT5, and MAP kinase 3, and a strong pathway relationship to IL-2 regulated genes which are known to govern cytotoxicity pathways. ChIP-seq analysis defined a canonical EBF4 binding motif 5’-CCCNNGG/AG-3’ closely related to the EBF1 binding site and using a luciferase-based reporter, we found a dose-dependent transcriptional response of this motif to EBF4. We also conducted ATAC-seq in EBF4 overexpressing cells and found increased chromatin accessibility upstream of granzyme and perforin and in topologically associated domains in human lymphocytes. Finally, we discovered that the EBF4 has basal expression in human but not mouse NK cells and CD8+ T cells and vanishes following activating stimulation. Together our data reveal key features of a previously unknown transcriptional regulator of human cytotoxic immune function.

2022-07-27 | GSE206220 | GEO

Increased Cell Surface Fas Expression is Necessary to Sensitize Lung Fibroblasts to Fas Ligation-Induced Apoptosis: Implications for Fibroblast Accumulation in Idiopathic Pulmonary Fibrosis.

Project description:Idiopathic pulmonary fibrosis (IPF) is associated with the accumulation of collagen-secreting fibroblasts and myofibroblasts in the lung parenchyma. Many mechanisms contribute to their accumulation, including resistance to apoptosis. In previous work, we showed that exposure to the pro-inflammatory cytokines, TNF-α and IFN-γ reverses fibroblast resistance to apoptosis. The goal of this study was to investigate the underlying mechanism. Based on an initial interrogation of the transcriptomes of unstimulated and TNF-α and IFN-γ-stimulated primary lung fibroblasts and the lung fibroblast cell line, MRC5, we show here that among Fas-signaling pathway molecules, Fas expression was increased ~6-fold in an NF-κB and p38mapk-dependent fashion. Prevention of the increase in Fas expression using Fas siRNAs blocked the ability of TNF-α and IFN-γ to sensitize fibroblasts to Fas ligation induced-apoptosis; while enforced adenovirus-mediated Fas overexpression was sufficient to overcome basal resistance to Fas-induced apoptosis. Examination of lung tissues from IPF patients revealed low to absent staining of Fas in fibroblastic cells of fibroblast foci. Collectively, these findings suggest that increased expression of Fas is necessary and sufficient to overcome the resistance of lung fibroblasts to Fas-induced apoptosis. They also suggest that approaches aimed at increasing Fas expression by lung fibroblasts and myofibroblasts may be therapeutically relevant. To investigate the mechanism by which TNF-α and IFN-γ reprogram fibroblasts from resistance to sensitivity to Fas-ligation-induce apoptosis, we exposed human primary lung fibroblasts from an IPF patient (FS087) and non-disease control subject (N78) and the human fetal lung fibroblast cell lung (MRC-5) to TNF-α (10 ng/ml) and IFN-γ (50 U/ml) for 36 hr and analyzed changes in their transcriptomes using Affymetrix microarrays.

2011-01-13 | E-GEOD-26594 | biostudies-arrayexpress

Increased Cell Surface Fas Expression is Necessary to Sensitize Lung Fibroblasts to Fas Ligation-Induced Apoptosis: Implications for Fibroblast Accumulation in Idiopathic Pulmonary Fibrosis.

2011-01-13 | GSE26594 | GEO

Early B Cell Factor 4 modulates FAS-mediated apoptosis and promotes cytotoxic function in human immune cells.

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

2022-07-27 | GSE206222 | GEO

Regulation of FAS Exon Definition and Apoptosis by the Ewing Sarcoma Protein

Project description:The EwingM-bM-^@M-^Ys sarcoma protein EWS belongs to the TET family (FUS/TLS, EWS, TAF15) of RNA and DNA binding proteins, implicated in DNA transcription, pre-mRNA splicing and maintenance of genomic integrity. Translocations of these genes are characteristic of particular neoplasias, including EwingM-bM-^@M-^Ys sarcoma. To identify physiological RNA targets of EWS, we performed in vivo cross-linking and immunoprecipitation followed by high-throughput RNA sequencing (HITS-CLIP/CLIP-Seq) in HeLa cells. Sequencing identified EWS binding sites characterized by guanosine-rich motifs in nearly 9000 genes, with particular enrichment in exonic regions near 5M-bM-^@M-^Y splice sites. Exon 6 of the Fas/CD95 receptor, which is alternatively spliced to generate isoforms with opposing activities in programmed cell death, was found as a prominent EWS CLIP target, as well as by chromatin-immunoprecipitation (ChIP) and functional analysis. Manipulation of EWS levels and mutation of EWS binding sites led to changes in alternative splicing consistent with EWS promoting exon 6 inclusion and leading to the synthesis of the pro-apoptotic Fas/CD95 isoform. Biochemical characterization of factors associated with FAS exon 6 are consistent with the notion that EWS binds to exonic sequences near the 5M-bM-^@M-^Y splice site and promotes the recruitment of U1snRNP, favoring also recognition of the upstream 3' splice site by U2AF and thus exon definition. Consistent with a role for EWS in the regulation of programmed cell death, cells depleted of EWS show decreased sensitivity to Fas-induced apoptosis. We discuss the potential implications of this novel function of EWS in EwingM-bM-^@M-^Ys sarcoma. CLIP-Seq analysis of EWS, with 2 biological replicates of EWS and one non-specific control

2014-05-21 | E-GEOD-48065 | biostudies-arrayexpress

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