Blockade of Y177 and Nuclear Translocation of Bcr-Abl Inhibits Proliferation and Promotes Apoptosis in Chronic Myeloid Leukemia Cells

The gradual emerging of resistance to imatinib urgently calls for the development of new therapy for chronic myeloid leukemia (CML). The fusion protein Bcr-Abl, which promotes the malignant transformation of CML cells, is mainly located in the cytoplasm, while the c-Abl protein which is expressed in...

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Détails bibliographiques
Auteurs principaux: Qianyin Li, Zhenglan Huang, Miao Gao, Weixi Cao, Qin Xiao, Hongwei Luo, Wenli Feng
Format: Artigo
Langue:Inglês
Publié: MDPI AG 2017-03-01
Collection:International Journal of Molecular Sciences
Sujets:
Bcr-Abl
nuclear
transport
proliferation
apoptosis
Accès en ligne:http://www.mdpi.com/1422-0067/18/3/537
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