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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...
Tallennettuna:
| Julkaisussa: | Int J Mol Sci |
|---|---|
| Päätekijät: | , , , , , , |
| Aineistotyyppi: | Artigo |
| Kieli: | Inglês |
| Julkaistu: |
MDPI
2017
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| Aiheet: | |
| Linkit: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5372553/ https://ncbi.nlm.nih.gov/pubmed/28257089 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.3390/ijms18030537 |
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