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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_4cellLines]

ABSTRACT: Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_4cellLines]

PROVIDER: PRJNA686294 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13271945_1.fastq.gz	Fastqsanger.gz
	SRR13271945_2.fastq.gz	Fastqsanger.gz
	SRR13271946_1.fastq.gz	Fastqsanger.gz
	SRR13271946_2.fastq.gz	Fastqsanger.gz
	SRR13271947_1.fastq.gz	Fastqsanger.gz

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia

Project description:Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_4cellLines]

Project description:Dysregulated gene expression is one of the most prevalent features in human cancers. Here, we show that most subtypes of acute myeloid leukemia (AML) depend on the aberrant assembly of the MYB transcriptional co-activator complex. By rapid and selective peptidomimetic interference with the binding of CBP/P300 to MYB, but not CREB or MLL1, we find that the leukemic functions of MYB are mediated by CBP/P300-mediated co-activation of a distinct set of transcriptional factor complexes that are aberrantly assembled with MYB in AML cells. This therapeutic remodeling is accompanied by dynamic redistribution of CBP/P300 complexes to genes that control cellular differentiation and growth. Thus, aberrantly organized transcription factor complexes control convergent gene expression programs in AML cells. These findings establish a compelling strategy for pharmacologic reprogramming of oncogenic gene expression that supports its targeting for leukemias and other human cancers caused by dysregulated gene control.

2021-02-24 | GSE163469 | GEO

Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_MV411]

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [ChIPseq]

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [ChIPseq]

Project description:Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [ChIPseq]

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Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_MV411]

Project description:Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia [RNAseq_MV411]

| PRJNA686277 | ENA

Definition of aberrant MYB CBP/P300 complex in AML

2020-12-17 | PXD019708 | Pride

Convergent organization of aberrant MYB complexes controls oncogenic gene expression in acute myeloid leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-24 | GSE163470 | GEO

MYB-regulated pancreatic cancer secretome

Project description:Earlier we have shown important roles of MYB in pancreatic tumor pathobiology. To better understand the role of MYB in the tumor microenvironment and identify MYB-associated secreted biomarker proteins, we conducted mass spectrometry analysis of the secretome from MYB-modulated and control pancreatic cancer cell lines. We also performed in silico analyses to determine MYB-associated biofunctions, gene networks and altered biological pathways. We further investigated the secreted proteins for their potential biomarker properties.

2021-09-08 | PXD015126 | Pride

MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.

2017-10-04 | PXD006857 | Pride

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