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ChIP-seq for RUNX1 and ETV6-RUNX1 in an induced pluripotent stem cell model of ETV6-RUNX1 pre-leukaemia

ABSTRACT: ChIP-seq for RUNX1 and ETV6-RUNX1 in an induced pluripotent stem cell model of ETV6-RUNX1 pre-leukaemia

PROVIDER: PRJEB57206 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10446973_1.fastq.gz	Fastqsanger.gz
	ERR10446973_2.fastq.gz	Fastqsanger.gz
	ERR10446974_1.fastq.gz	Fastqsanger.gz
	ERR10446974_2.fastq.gz	Fastqsanger.gz
	ERR10446975_1.fastq.gz	Fastqsanger.gz

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ChIP-seq for RUNX1 and ETV6-RUNX1 in an induced pluripotent stem cell model of ETV6-RUNX1 pre-leukaemia

Project description:ETV6-RUNX1 is a first-hit mutation in childhood B cell precursor acute lymphoblastic leukaemia. ETV6-RUNX1 is a fusion protein which inherits the DNA-binding runt domain from RUNX1. Here we performed chromatin precipitation for native RUNX1 and ETV6-RUNX1 using RUNX1 antibodies and specifically for the ETV6-RUNX1 fusion using a V5-tag pull down.

2022-10-31 | E-MTAB-12208 | biostudies-arrayexpress

Histone H3, lysine 27 acetylation ChIP-seq in NALM6 expressing ETV6-RUNX1

Project description:ETV6-RUNX1 is a fusion protein bringing together almost the entire coding sequence of RUNX1, including the DNA binding runt domain, and the N-terminus of ETV6 which is known to include transcriptional repressors including histone deacetylation 3 (HDAC3). Here we perform ChIP-seq for the active chromatin mark H3K27ac in the NALM6 B-cell acute lymphoblastic leukaemia cell line expressing ETV6-RUNX1 or mutant derivatives of ETV6-RUNX1: Delta helix-loop-helix (dHLH) is a deletion of the pointed domain; R139G is a point mutation in the runt DNA-binding domain.

2022-10-31 | E-MTAB-12207 | biostudies-arrayexpress

Whole-genome mapping of ETV6-RUNX1 in pre-B lymphoblast models

Project description:Genome binding/occupancy profiling of ETS Variant Transcription Factor 6- Runt Related Transcription Factor 1 fusion protein (ETV6-RUNX1) in REH cells by high throughput sequencing. ETV6-RUNX1 is expressed in pediatric t(12;21) ETV6-RUNX1 B cell precursor acute lymphoblastic leukemia.

2022-04-01 | GSE176084 | GEO

Identification of ETV6/RUNX1 regulated lncRNAs

Project description:Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their expression and role in pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1 positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. An ETV6/RUNX1 expression signature was established, consisting of 596 lncRNAs (434 up and 162 down) using expression analysis of a series of primary patient samples. Subsequently, RNA sequencing from BCP-ALL cell lines and shRNA-mediated silencing of ETV6/RUNX1, illustrated that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are bona fide ETV6/RUNX1 targets and could serve as novel biomarkers of this prevalent subtype of human leukemia.

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Insights into inherited thrombocytopenia resulting from mono-allelic germline mutations in ETV6 or RUNX1 using a human pluripotent stem cell model

Project description:Inherited thrombocytopenia results in low platelet counts and increased bleeding. Subsets of these patients have monoallelic germline mutations in ETV6 or RUNX1 and a heightened risk of developing hematologic malignancies. Utilizing CRISPR/Cas9, we compared the in vitro phenotype of hematopoietic progenitor cells and megakaryocytes derived from induced pluripotent stem cell (iPSC) lines harboring mutations in either ETV6 or RUNX1. Both mutant lines display phenotypes consistent with a platelet-bleeding disorder. Surprisingly, these cellular phenotypes were largely distinct. The ETV6-mutant iPSCs yield more hematopoietic progenitor cells and megakaryocytes, but the megakaryocytes are immature and less responsive to agonist stimulation. On the contrary, RUNX1-mutant iPSCs yield fewer hematopoietic progenitor cells and megakaryocytes, but the megakaryocytes are more responsive to agonist stimulation. However, both mutant iPSC lines display defects in proplatelet formation. Our work highlights that while patients harboring germline ETV6 or RUNX1 mutations have similar clinical phenotypes, the molecular mechanisms may be distinct.

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Loss of BTG1 function promotes ETV6-RUNX1-mediated leukemic transformation by upregulation of BCL6

Project description:Analysis of gene signatures in WT+Ctrl vs WT+ETV6-RUNX1, Btg1-/- and Btg1-/-+ETV6-RUNX1 in cKit+Ter119- fetal liver-derived hematopoietic progenitor cells (FL-HPCs). The Btg1-/-+ETV6-RUNX1 FL-HPCs display a strong increase in proliferation compared to WT+ETV6-RUNX1. Total RNA otained from WT+Ctrl, WT+ETV6-RUNX1, Btg1-/-+Ctrl and Btg1-/-+ETV6-RUNX1 FL-HPCs cells that were cultured for 12 days in expansion medium.

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Whole-genome mapping of ETV6-RUNX1 in pre-B lymphoblast models

Project description:Whole-genome mapping of ETV6-RUNX1 in pre-B lymphoblast models

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ChIP-seq for RUNX1 and ETV6-RUNX1 in B-ALL cell lines and patient samples

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ChIP-seq in the cell line NALM-6 for RUNX1 and ETV6-RUNX1 to assess competition between the two proteins for DNA binding

Project description:RUNX1 and ETV6-RUNX1 possess the same DNA-binding runt domain and are therefore expected to bind to canonical RUNX motifs. As the ETV6-RUNX1 fusion arises in the context of native RUNX1 expression, and since RUNX1 is retained or amplified in B-ALL, the two proteins are likely to compete for the same target sites. To assess this, we performed RUNX1 ChIP-seq in the presence of exogenous ETV6-RUNX1 (or non DNA binding ETV6-RUNX1-R139G) and the reciprocal experiment: ETV6-RUNX1 ChIP (using a V5 tag) in the presence of exogenous RUNX1 or vector control.

2022-10-31 | E-MTAB-12209 | biostudies-arrayexpress

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