Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/5101
Title: Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells
Authors: Can, Geylani
Ekiz, Hüseyin Atakan
Baran, Yusuf
Keywords: ATG genes
Autophagy
Chronic myeloid leukemia
Imatinib
BECLIN 1 gene
Publisher: Taylor and Francis Ltd.
Source: Can, G., Ekiz, H.A., and Baran, Y. (2011). Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells. Hematology, 16(2), 95-99. doi:10.1179/102453311X12902908412039
Abstract: Locate full-text(opens in a new window)|Full Text(opens in a new window)|View at Publisher| Export | Download | Add to List | More... Hematology Volume 16, Issue 2, March 2011, Pages 95-99 Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells (Article) Can, G., Ekiz, H.A., Baran, Y. Department of Molecular Biology and Genetics, Faculty of Science, Izmir Institute of Technology, 35430 Urla, Izmir, Turkey View references (35) Abstract Imatinib is a chemotherapeutic drug used for the treatment of chronic myeloid leukemia (CML). Recent data showed imatinib-induced cell death in various types of cancers. Autophagy is the physiological process in which cellular components are broken down by the lysosomal activation. In this study, we aimed to examine the effects of imatinib on autophagy in addition to apoptosis in CML cells. Results suggested that imatinib induces autophagy in CML cells through inducing over-expression of BECLIN-1 and ATG5 genes with the statistical significance. Our results demonstrated that autophagy might be involved in imatinib-induced cell death.
URI: https://doi.org/10.1179/102453311X12902908412039
http://hdl.handle.net/11147/5101
ISSN: 1024-5332
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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