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The role of Erg in B cell development (ATAC-Seq)

ABSTRACT: The role of Erg in B cell development (ATAC-Seq)

PROVIDER: PRJNA549274 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9311840_1.fastq.gz	Fastqsanger.gz
	SRR9311840_2.fastq.gz	Fastqsanger.gz
	SRR9311841_1.fastq.gz	Fastqsanger.gz
	SRR9311841_2.fastq.gz	Fastqsanger.gz
	SRR9311835_1.fastq.gz	Fastqsanger.gz

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The role of Erg in B cell development (ChIP-Seq)

Project description:The role of Erg in B cell development (ChIP-Seq)

| PRJNA549273 | ENA

The role of Erg in B cell development (RNA-Seq)

Project description:The role of Erg in B cell development (RNA-Seq)

| PRJNA549275 | ENA

ERG controls B-cell development by promoting Igh V-to-DJ recombination [ATAC-seq]

Project description:ERG controls B-cell development by promoting Igh V-to-DJ recombination [ATAC-seq]

| PRJNA529613 | ENA

ERG controls B-cell development by promoting Igh V-to-DJ recombination [ATAC-seq]

Project description:B-cell development is dependent on the coordinated expression and cooperation of several transcription factors. Here, we show that the transcription factor ETS Related Gene (ERG) is crucial for normal B-cell development, and that its deletion results in a substantial loss of bone marrow B-cell progenitors and peripheral B-cells as well as a skewing of splenic B-cell populations. We found that ERG-deficient B-lineage cells exhibited an early developmental block, at the pre-B cell stage, and proliferated less. The cells failed to express the immunoglobulin heavy chain due to inefficient V-to-DJ recombination and cells that managed to undergo recombination displayed a strong bias against incorporation of distal V gene segments. Furthermore, antisense transcription at PAX5-activated intergenic repeat (PAIR) elements located in the distal region of the Igh locus was completely dependent on ERG. These findings identify ERG as a novel critical regulator of B-cell development by ensuring efficient and balanced V-to-DJ recombination.

2019-11-24 | GSE128975 | GEO

The role of Erg in B cell development (ATAC-Seq)

Project description:ATAC-seq of pre-proB, proB and preB populations from Ergfl/fl bone marrow, pre-proB cell population from Rag1CreT/+;ErgΔ/Δ bone marrow, and pre-proB, proB and preB populations from from Rag1CreT/+;ErgΔ/Δ;IgHVH10tar bone marrow.

2020-04-14 | GSE132852 | GEO

The role of Erg in B cell development (ChIP-Seq)

Project description:ChIP-seq of B-cell progenitors and Rag1CreT/+;ErgΔ/Δ thymocytes for Erg transcription factor

2020-04-14 | GSE132853 | GEO

Development of peptidomimetic inhibitors of the ERG transcription factor in prostate cancer (ChIP-seq)

Project description:Transcription factors play a key role in the development of a number of cancers, and therapeutically targeting them has remained a challenge. In prostate cancer, the ETS transcription factor ERG is recurrently rearranged and likely plays a critical role in prostate oncogenesis. Here we identified a series of peptides from a phage-display library that interact specifically with the DNA binding domain of ERG. The interactive interface was mapped to 9-residues in the 3rd helix of the ETS domain that is critical for ERG transcriptional activity. The peptides were found to efficiently disrupt ERG-mediated protein-protein interactions, transcription, DNA damage, and cell invasion, as well as attenuate ERG recruitment to target gene loci. Furthermore, a retroinverso peptidomimetic version of the peptide sequence suppressed tumor growth, intravasation, and metastasis in vivo. Taken together, our results demonstrate that transcription factors have specific residues important for protein-protein interactions and disrupting those critical interactions may be an effective therapeutic strategy. Examination of ERG in VCaP cells with respect to peptidomimetics treatment

2014-07-15 | E-GEOD-58939 | biostudies-arrayexpress

Development of peptidomimetic inhibitors of the ERG transcription factor in prostate cancer (ChIP-seq)

2014-07-15 | GSE58939 | GEO

ERG controls B-cell development by promoting Igh V-to-DJ recombination [RNA-seq]

2019-11-24 | GSE128977 | GEO

Epigenome-wide impact of MAT2A sustains the androgen-indifferent state and confers synthetic vulnerability in ERG fusion-positive prostate cancer

Project description:Castration-resistant prostate cancer (CRPC) is a frequently occurring disease with adverse clinical outcomes and limited therapeutic options. Here, we identify a novel role of methionine adenosyltransferase 2a (MAT2A) as a driver of the androgen-indifferent state in ERG fusion-positive CRPC. We show that MAT2A is upregulated in CRPC and cooperates with ERG in promoting cell plasticity, stemness and tumorigenesis. RNA, ATAC and ChIP sequencing coupled with mass spectrometry analysis of histone post-translational modifications show that MAT2A broadly impacts the transcriptional and epigenetic landscape. MAT2A enhances H3K4me2 at multiple genomic sites promoting the expression of pro-tumorigenic non-canonical AR target genes in CRPC models. Genetic and pharmacological inhibition of MAT2A in preclinical models reversed this transcriptional and epigenetic remodeling, promoting luminal differentiation and improving the response to AR and EZH2 inhibitors. This data reveals a previously unrecognized function of MAT2A in epigenetic reprogramming and a synthetic vulnerability to MAT2A inhibitors in ERG fusion-positive CRPC.

2024-06-06 | PXD042895 | Pride

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