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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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Detalles Bibliográficos
Autores principales: Li, Qianyin, Huang, Zhenglan, Gao, Miao, Cao, Weixi, Xiao, Qin, Luo, Hongwei, Feng, Wenli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5372553/
https://www.ncbi.nlm.nih.gov/pubmed/28257089
http://dx.doi.org/10.3390/ijms18030537

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