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Mus musculus

ABSTRACT: Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [EBF1]

PROVIDER: PRJNA155693 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR409118.fastq.gz	Fastqsanger.gz
	SRR409119.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells

Project description:This SuperSeries is composed of the following subset Series: GSE35910: Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [EBF1] GSE35914: Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [H3K4me2 and H3K4me3] Refer to individual Series See related Series GSE36061.

2012-04-02 | E-GEOD-35915 | biostudies-arrayexpress

Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells

Project description:Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells

| PRJNA152013 | ENA

Mus musculus

Project description:Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [H3K4me2 and H3K4me3]

| PRJNA155699 | ENA

Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [EBF1]

Project description:Transcription factor Ebf1 is an important determinant of early B lymphopoiesis. To gain insight into differentiation stage-specific functions of Ebf1, we conditionally inactivated Ebf1. We found that Ebf1 is required for proliferation, survival and signaling of pro-B cells and peripheral B cell subsets. The proliferation defect of Ebf1-deficient pro-B cells, including the impaired expression of IL-7Ra and several cell cycle regulators, is overcome by transformation with v-Abl. The survival defect of transformed Ebf1fl/fl pro-B cells can be rescued by the forced expression of the Ebf1 targets c-Myb or Bcl-xL. In mature B cells, Ebf1 deficiency interferes with the BAFF-R and BCR-dependent Akt signaling pathways, as well as with germinal center formation and class switch recombination. Genome-wide analyses of Ebf1 binding and Ebf1-mediated gene expression in mature B cells and comparison with reported data sets in pro-B cells provide insight into the basis for lineage- and stage-specific functions of Ebf1. EBF1 binding in splenic B cells in mice

2012-04-02 | E-GEOD-35910 | biostudies-arrayexpress

Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [H3K4me2 and H3K4me3]

2012-04-02 | E-GEOD-35914 | biostudies-arrayexpress

A comprehensive Proteomic Investigation of Ebf1 Heterozygosity in pro-B lymphocytes utilizing Data Independent Acquisition

Project description:Early B cell factor 1 (EBF1) is one of the key transcription factors required for orchestrating B-cell lineage development. Although studies have shown that Ebf1 haploinsufficiency is involved in the development of leukemia, no study has been conducted that characterizes the global effect of Ebf1 heterozygosity on the proteome of pro-B lymphocytes. Here, we employ both DIA (Data Independent Acquisition) and shotgun DDA (Data Dependent Acquisition) workflows for profiling proteins that are differently expressed between Ebf1+/+ and Ebf1+/- cells. Both DDA and DIA were able to reveal the downregulation of the EBF1 transcription factor in Ebf1+/- pro-B lymphocytes. Further examination of differentially expressed proteins by DIA revealed that, similar to EBF1, the expression of other B-cell lineage regulators, such as TCF3 and Pax5, is also down-regulated in Ebf1 heterozygous cells. Functional DIA analysis of differentially expressed proteins showed that EBF1 heterozygosity resulted in the deregulation of at least 8 transcription factors involved in lymphopoiesis, and to the deregulation of key proteins playing crucial roles in survival, development and differentiation of pro-B lymphocytes.

2017-12-20 | PXD008396 | Pride

Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [EBF1]

2012-04-03 | GSE35910 | GEO

Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferative expansion and survival of B cells [H3K4me2 and H3K4me3]

2012-04-03 | GSE35914 | GEO

Transcription factor EBF1 non-cell autonomously regulates cardiac growth and differentiation

Project description:Transcription factor EBF1 non-cell autonomously regulates cardiac growth and differentiation

| PRJNA1016462 | ENA

Chromatin restriction by the nucleosome remodeler Mi-2β and functional interplay with lineage-specific transcription regulators controls B cell differentiation

Project description:Coordinated induction but also repression of genes is key to normal differentiation. Although the role of lineage-specific transcription regulators has been extensively studied, their functional integration with chromatin remodelers, one of the key enzymatic machineries that control chromatin accessibility, remains ill-defined. Here we investigate the role of Mi-2b, a SNF-2-like nucleosome remodeler and key component of the Nucleosome Remodeling Deacetylase (NuRD) complex in early B cells. Inactivation of Mi-2b arrested differentiation at the large pre-B cell stage and caused de-repression of cell adhesion and cell migration signaling factors by increasing chromatin access at poised enhancers and chromosome architectural elements. Mi-2b also supported IL-7R signaling, survival and proliferation by repressing negative effectors of this pathway. Importantly, over-expression of Bcl2, a mitochondrial pro-survival factor and target of IL-7R signaling, partly rescued the differentiation block caused by Mi-2b loss. Mi-2b stably associated with chromatin sites that harbor binding motifs for IKAROS and EBF1 and physically associated with these transcription factors both on and off chromatin. Notably, Mi-2b shared loss-of-function cellular and molecular phenotypes with IKAROS and EBF1 albeit in a distinct fashion. Thus the nucleosome remodeler Mi-2b promotes pre-B cell differentiation by providing repression capabilities to distinct lineage-specific transcription factor-based regulatory networks.

2019-05-15 | GSE130315 | GEO

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