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Article

Disruption of the NHR4 domain structure in AML1-ETO abrogates SON binding and promotes leukemogenesis

24 Oct 2008

Abstract excerpt

AML1-ETO is generated from t(8;21)(q22;q22), which is a common form of chromosomal translocation associated with development of acute myeloid leukemia (AML). Although full-length AML1-ETO alone fails to promote leukemia because of its detrimental effects on cell proliferation, an alternatively spliced isoform, AML1-ETO9a, without its C-terminal NHR3/NHR4 domains, strongly induces leukemia. However, full-length...

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PMID: 18952841
DOI: 10.1073/pnas.0802696105

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