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Differential tyrosine phosphorylation of leukemic cells during apoptosis as a result of treatment with imatinib mesylate
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- Authors
- Issue Date
- 2005-09-15
- Publisher
- Elsevier
- Citation
- Biochem Biophys Res Commun. 2005 Oct 28;336(3):942-51.
- Keywords
- Antineoplastic Agents/*pharmacology ; Blotting, Western ; Cell Cycle/drug effects ; Cell Cycle Proteins/genetics/metabolism ; Cell Proliferation/drug effects ; Electrophoresis, Gel, Two-Dimensional ; Fusion Proteins, bcr-abl/*antagonists & inhibitors ; Humans ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL ; Positive/*enzymology/metabolism/pathology ; Phosphorylation ; Piperazines/*pharmacology ; Protein Kinase Inhibitors/*pharmacology ; Proteome/metabolism ; Pyrimidines/*pharmacology ; Transcription, Genetic/drug effects ; Tyrosine/metabolism ; Apoptosis
- Abstract
- Bcr-Abl fusion tyrosine kinase contributes to leukemic transformation. Imatinib mesylate inhibits Bcr-Abl tyrosine kinase, resulting in a blockage of tyrosine phosphorylation in its downstream pathways. We analyzed the alteration of tyrosine phosphorylation, on BCR/ABL+ chronic myelogenous leukemia cells, after treatment with imatinib mesylate. Data were collected using a two-dimensional gel electrophoresis followed by Western blot and mass spectrometry. The inhibition of Bcr-Abl tyrosine kinase by 2.5 microM imatinib mesylate caused both cell cycle arrest in the G0/G1 phase and increased the portion of apoptotic cells. As a result, the population of leukemic cells decreased by 30% and 70% compared to controls at 24 and 72 h, respectively. Furthermore, treatment with imatinib mesylate altered tyrosine phosphorylation of 24 protein spots as the incubation time proceeded from 0 to 24 and 72 h. Ten of the 24 protein spots are visible at all three times. Four are detectable at both the 0 and 24 h points in time. Eight were detectable only at time 0.
- ISSN
- 0006-291X (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16157305
http://dx.dor.org/10.1016/j.bbrc.2005.08.201
https://hdl.handle.net/10371/47067
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