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ATACSeq and genome-wide binding profile of EBF1 and Pax5 to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice.

ABSTRACT: ATACSeq and genome-wide binding profile of EBF1 and Pax5 to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice.

PROVIDER: PRJNA666169 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12730751_1.fastq.gz	Fastqsanger.gz
	SRR12730751_2.fastq.gz	Fastqsanger.gz
	SRR12730752_1.fastq.gz	Fastqsanger.gz
	SRR12730752_2.fastq.gz	Fastqsanger.gz
	SRR12730753_1.fastq.gz	Fastqsanger.gz

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ATACSeq and genome-wide binding profile of EBF1 and Pax5 to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice.

Project description:ATACSeq, EBF1 ChIPSeq and Pax5 ChIPSeq of dHet B-ALL, dHet proB and wt proB cells.

2020-10-19 | GSE158671 | GEO

Single-cell RNASeq analysis to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice

Project description:Here, we report that EBF1 and Pax5 collaborate in a dose-dependent manner to regulate the IL-7-STAT5 signaling pathway and one-carbon metabolism, whereby we found both diminished and enhanced binding of EBF1 and Pax5 to target genes in compound heterozygous mutant mice. Moreover, single-cell RNA sequencing analysis identified a small subset of wild-type pro-B cells on the trajectory to pre-B cells that share gene expression signatures with leukemic Ebf1+/−Pax5+/− pro-B cells. Thus, a normal expression level of EBF1 and Pax5 is required for safeguarding a potentially vulnerable pro-Bcell subset from a transformation to B-ALL.

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Microarray analysis to unravel molecular networks driving leukemia in Ebf1+/- Pax5+/- (dHet) B-ALL mice

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RNASeq analysis to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice

Project description:RNASeq analysis to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice

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RNASeq analysis to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice

Project description:To profile gene expression changes in Ebf1+/-Pax5+/- (dHet) leukemic mice, we performed RNASeq analysis in dHet B-ALL, dHet proB and wt proB cells.

2020-10-19 | GSE158661 | GEO

Microarray analysis to unravel molecular networks driving leukemia in Ebf1+/- Pax5+/- (dHet) B-ALL mice

Project description:To profile gene expression changes in Ebf1+/-Pax5+/- (dHet) B-ALL mice, we performed microarray analysis in dHet B-ALL, dHet proB and wt proB cells

2020-10-19 | GSE158645 | GEO

Single-cell RNASeq analysis to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice

Project description:Single-cell RNASeq analysis to unravel molecular networks driving leukemia in Ebf1+/-Pax5+/- (dHet) B-ALL mice

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Expression data comparing EBF1 versus Pax5 induced genes

Project description:We used microarrays to establish whether EBF1 and Pax5 repress similar or unique genes. We found that EBF1 uniquely represses the expression of the T-lineage transcription factor Gata3. Ebf1-/- pre-pro-B cells were transduced with either control MigR1, MigY-EBF1 or MigR-Pax5 viruses. 24 hours later, RNA was isolated and processed for Affymetrix microarray analysis. Cells expressing EBF1, Pax5, or neither were sorted and processed. Scale represents log2 value of normalized signal level.

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Ebf1 or Pax5 Haploinsufficiency Synergizes with STAT5 Activation to Initiate Acute Lymphoblastic Leukemia

Project description:STAT5 is critical for differentiation, proliferation and survival of progenitor B cells suggesting a possible role in Acute Lymphoblastic Leukemia (ALL). Herein, we show increased expression of activated STAT5 in ALL patients, which correlates with treatment outcome. Mutations in Ebf1 and Pax5, genes critical for B cell development have also been identified in human ALL. To determine whether mutations in Ebf1 or Pax5 synergize with STAT5 activation to induce ALL we crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) with mice heterozygous for Ebf1 or Pax5. Haploinsufficiency of either Pax5 or Ebf1 synergized with Stat5b-CA to rapidly induce ALL in 100% of the mice. The leukemic cells displayed reduced expression of both Pax5 and Ebf1 but this had little affect on most EBF1 or PAX5 target genes. However, a subset of these genes was deregulated and included a large percentage of potential tumor suppressor genes and oncogenes. Further, most of these genes appear to be jointly regulated by both EBF1 and PAX5. Our findings suggest a model whereby small perturbations in a self-reinforcing network of transcription factors critical for B cell development, specifically PAX5 and EBF1, cooperate with STAT5 activation to initiate ALL. Gene expression profiling was performed on cells isolated from lymph nodes of Stat5b-CA x Ebf1+/- and Stat5b-CA x Rag2-/- leukemic mice and pre B cells sorted from bone marrow of C57BL/6 mice and Stat5b-CA transgenic mice. 17 Samples.

2011-05-09 | E-GEOD-25645 | biostudies-arrayexpress

Ebf1 or Pax5 Haploinsufficiency Synergizes with STAT5 Activation to Initiate Acute Lymphoblastic Leukemia

2011-05-09 | GSE25645 | GEO