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

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 splic...

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Autores principales: Ahn, Eun-Young, Yan, Ming, Malakhova, Oxana A., Lo, Miao-Chia, Boyapati, Anita, Ommen, Hans Beier, Hines, Robert, Hokland, Peter, Zhang, Dong-Er
Formato: Artigo
Lenguaje:Inglês
Publicado: National Academy of Sciences 2008
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Acceso en línea:https://ncbi.nlm.nih.gov/pmc/articles/PMC2579385/
https://ncbi.nlm.nih.gov/pubmed/18952841
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0802696105
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