The use of isobaric tag peptide labeling (iTRAQ) and mass spectrometry to examine rare, primitive hematopoietic cells from patients with ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-04-19

AUTHORS

Stephen D. Griffiths, John Burthem, Richard D. Unwin, Tessa L. Holyoake, Junia V. Melo, Guy S. Lucas, Anthony D. Whetton

ABSTRACT

Chronic Myeloid Leukemia (CML) is a hematopoietic stem cell disease, associated with a t(9, 22) chromosomal translocation leading to formation of the BCR/ABL chimeric protein, which has an intrinsic tyrosine kinase activity. Recently, the BCR/ABL tyrosine kinase inhibitor imatinib mesylate (imatinib) has been successfully used clinically, although, disease relapse can still occur. The precise detail of the mechanism by which CML cells respond to imatinib is still unclear. We therefore systematically examined the effects of imatinib on the primitive CML cell proteome, having first established that the drug inhibits proliferation and induces increased apoptosis and differentiation. To define imatinib-induced effects on the CML proteome, we employed isobaric tag peptide labeling (iTRAQ) coupled to two-dimensional liquid chromatography/tandem mass spectrometry. Given the limited clinical material available, the isobaric tag approach identified a large population of proteins and provided relative quantification on four samples at once. Novel consequences of the action of imatinib were identified using this mass spectrometric approach. DEAD-box protein 3, heat shock protein 105 kDa, and peroxiredoxin-3 were identified as potential protein markers for response to imatinib. More... »

PAGES

81-89

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12033-007-0005-5

DOI

http://dx.doi.org/10.1007/s12033-007-0005-5

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17914187


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43 schema:description Chronic Myeloid Leukemia (CML) is a hematopoietic stem cell disease, associated with a t(9, 22) chromosomal translocation leading to formation of the BCR/ABL chimeric protein, which has an intrinsic tyrosine kinase activity. Recently, the BCR/ABL tyrosine kinase inhibitor imatinib mesylate (imatinib) has been successfully used clinically, although, disease relapse can still occur. The precise detail of the mechanism by which CML cells respond to imatinib is still unclear. We therefore systematically examined the effects of imatinib on the primitive CML cell proteome, having first established that the drug inhibits proliferation and induces increased apoptosis and differentiation. To define imatinib-induced effects on the CML proteome, we employed isobaric tag peptide labeling (iTRAQ) coupled to two-dimensional liquid chromatography/tandem mass spectrometry. Given the limited clinical material available, the isobaric tag approach identified a large population of proteins and provided relative quantification on four samples at once. Novel consequences of the action of imatinib were identified using this mass spectrometric approach. DEAD-box protein 3, heat shock protein 105 kDa, and peroxiredoxin-3 were identified as potential protein markers for response to imatinib.
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51 DEAD box protein 3
52 action
53 action of imatinib
54 activity
55 apoptosis
56 approach
57 cell disease
58 cell proteome
59 cells
60 chimeric protein
61 chromosomal translocations
62 chronic myeloid leukemia
63 clinical material
64 consequences
65 detail
66 differentiation
67 disease
68 disease relapse
69 drugs
70 effect
71 effects of imatinib
72 formation
73 hematopoietic cells
74 hematopoietic stem cell disease
75 imatinib
76 imatinib mesylate
77 inhibitor imatinib mesylate
78 intrinsic tyrosine kinase activity
79 kDa
80 kinase activity
81 kinase inhibitor imatinib mesylate
82 labeling
83 large population
84 leukemia
85 limited clinical material
86 liquid chromatography/tandem mass spectrometry
87 markers
88 mass spectrometric approach
89 mass spectrometry
90 materials
91 mechanism
92 mesylate
93 myeloid leukemia
94 novel consequences
95 patients
96 peptide labeling
97 peroxiredoxin 3
98 population
99 potential protein markers
100 precise details
101 primitive hematopoietic cells
102 proliferation
103 protein
104 protein 3
105 protein markers
106 proteome
107 quantification
108 relapse
109 relative quantification
110 response
111 samples
112 spectrometric approach
113 spectrometry
114 stem cell disease
115 tag approach
116 tandem mass spectrometry
117 translocation
118 two-dimensional liquid chromatography/tandem mass spectrometry
119 tyrosine kinase activity
120 tyrosine kinase inhibitor imatinib mesylate
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