BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein

Recent studies have revealed that p27, a nuclear cyclin-dependent kinase (Cdk) inhibitor and tumor suppressor, can acquire oncogenic activities upon mislocalization to the cytoplasm. To understand how these antagonistic activities influence oncogenesis, we dissected the nuclear and cytoplasmic funct...

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Veröffentlicht in:	Blood 2014-11, Vol.124 (22), p.3260-3273
Hauptverfasser:	Agarwal, Anupriya, Mackenzie, Ryan J., Besson, Arnaud, Jeng, Sophia, Carey, Alyssa, LaTocha, Dorian H., Fleischman, Angela G., Duquesnes, Nicolas, Eide, Christopher A., Vasudevan, Kavin B., Loriaux, Marc M., Firpo, Eduardo, Cortes, Jorge E., McWeeney, Shannon, O’Hare, Thomas, Roberts, James M., Druker, Brian J., Deininger, Michael W.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cell Transformation, Neoplastic - genetics Cells, Cultured Cyclin-Dependent Kinase Inhibitor p27 - metabolism Cytoplasm - metabolism Fusion Proteins, bcr-abl - physiology Genes, Tumor Suppressor Humans Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Mice Mice, Inbred C57BL Mice, Transgenic Myeloid Neoplasia Oncogene Proteins - metabolism Protein Transport - genetics
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