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ATAC-seq analysis for HPB-ALL cells overexprssing TAL1 and LMO1.

ABSTRACT: ATAC-seq analysis for HPB-ALL cells overexprssing TAL1 and LMO1.

PROVIDER: PRJNA939155 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23636201_1.fastq.gz	Fastqsanger.gz
	SRR23636201_2.fastq.gz	Fastqsanger.gz
	SRR23636202_1.fastq.gz	Fastqsanger.gz
	SRR23636202_2.fastq.gz	Fastqsanger.gz
	SRR23636203_1.fastq.gz	Fastqsanger.gz

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ATAC-seq analysis for HPB-ALL cells overexprssing TAL1 and LMO1.

Project description:ATAC-seq analysis was performed in a T-ALL cell line (HPB-ALL) which overexpresses TAL1 and LMO1 to analyze chromatin accessibility.

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RNA-seq analysis after TAL1 and LMO1 overexpression in HPB-ALL cells

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RNA-seq analysis after TAL1 and LMO1 overexpression in HPB-ALL cells

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Project description:The TAL1/SCL and LMO1 oncogenic transcription factors establish a pre-leukemic state by reprogramming thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Pre-TCR signaling accelerates the progression to T-cell acute lymphoblastic leukemia (T-ALL). To directly address the importance of pre-TCR signaling in driving progression to T-ALL, we leverage on Cd3-deficient mice in which pre-TCR signaling and progression through β-selection is abrogated. In the absence of pre-TCR signaling in Cd3ε-deficient SCL-LMO1 transgenic mice, T-ALL onset is delayed by 150 days. Despite the absence of pre-TCR/CD3 signaling in these mice, we show that leukemic thymocytes exhibit the gene expression profiles of thymocytes that have undergone β-selection, i.e. exhibiting a re-activation of pre-TCR-driven proliferation signature, and a down regulation of HEB/TCF12 target genes. Lastly, monoallelic deletion of Heb is sufficient to accelerate T-ALL onset in Cd3ε-deficient SCL-LMO1 transgenic mice. Together, these results underscore the role of HEB/TCF12 as a tumor suppressor in T-ALL.

2022-03-27 | GSE198506 | GEO

ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells

Project description:The oncogenic transcription factor TAL1/SCL is aberrantly expressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing its importance in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, LMO1, LMO2, GATA3 and RUNX1 in T-ALL cells. We show that TAL1 forms an interconnected auto-regulatory loop with its partners, and that the TAL1 complex directly activates the MYB oncogene, forming a feed-forward positive regulatory loop that further promotes the TAL1-regulated oncogenic program. one of the cirtical downstream targets in this circuitry is the TRIB2 gene, which is oppositely regulated by TAL1 and HEB/E2A, and is essential for the survival of T-ALL cells. Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), LMO1 (Santa Cruz SC-10494), LMO2 (R&D AF2726),GATA3 (Santa Cruz SC-22206) and RUNX1 (Santa Cruz SC-8563). This represents the ChIP-seq portion of this dataset.

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ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells

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Project description:The SCL and LMO1 oncogenic transcription factors reprogram thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Here we report that SCL directly interacts with LMO1 to activate the transcription of a self-renewal program coordinated by LYL1. Gene expression profiles of thymocytes from SCL-LMO1 transgenic and age-matched non transgenic Cd3Îµ-/- mice were compared to identify candidate genes that confer self-renewal capability to pre-leukemic thymocytes.

2015-11-05 | E-GEOD-74659 | biostudies-arrayexpress

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Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries)

Project description:The oncogenic transcription factor TAL1/SCL is aberrantly overexpressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing the importance of the TAL1-regulated transcriptional program in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, GATA3, ETS1 and RUNX1 in T-ALL cells. We find that TAL1 forms an interconnected auto-regulatory loop with its partners, which contributes to the sustained upregulation of its direct target genes. Importantly, we also find the MYB oncogenic transcription factor is directly activated by the TAL1 complex and positively regulates many of the same target genes, thus forming a feed-forward positive regulatory loop that further promotes the TAL1-regulated oncogenic program. Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), LMO1 (Santa Cruz SC-10494), LMO2 (R&D Systems AF2726), GATA3 (Santa Cruz SC-22206) and RUNX1 (Santa Cruz SC-8563). This represents the ChIP-seq portion of this dataset. Human Jurkat cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), LMO1 (Santa Cruz SC-10494), GATA3 (Santa Cruz SC-22206) and RUNX1 (Santa Cruz SC-8563). This represents the ChIP-seq portion of this dataset.

2012-03-14 | E-GEOD-33850 | biostudies-arrayexpress

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