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Article

Depletion of RUNX1/ETO in t(8;21) AML cells leads to genome-wide changes in chromatin structure and transcription factor binding.

Leukemia - 1 Aug 2012

Ptasinska A, Assi S A, Mannari D, James S R, Williamson D, Dunne J, Hoogenkamp M, Wu M, Care M, McNeill H, Cauchy P, Cullen M, Tooze R M, Tenen D G, Young B D, Cockerill P N, Westhead D R, Heidenreich O, Bonifer C

Abstract excerpt

The t(8;21) translocation fuses the DNA-binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The result of this interference is a block in differentiation and, finally, the development of acute myeloid leukemia (AML). To obtain insights into RUNX1/ETO-dependant...

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Share to Acetylation
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromosomes, Human, Pair 21

Share to Chromosomes, Human, Pair 8

Share to Core Binding Factor Alpha 2 Subunit

Share to Oncogene Proteins, Fusion

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Source

Open in PubMed Open full text

Identifiers

PMID: 22343733
DOI: 10.1038/leu.2012.49
PMCID: PMC3419980

Genes

RUNX1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

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Depletion of RUNX1/ETO in t(8;21) AML cells leads to genome-wide changes in chromatin structure and transcription factor binding.PMID 22343733Read ↗

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