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Biochemistry and Biophysics |
Departments of Molecular and Cell Biology and Chemistry and Howard Hughes Medical Institute, University of California, Berkeley, California 94720 [B. N., P. P., J. K.]; Physical Biosciences Division, Lawrence Berkeley National Lab, Berkeley, California 94720 [B. N., P. P., J. K.]; Memorial Sloan-Kettering Cancer Center, New York, New York 10021 [W. G. B., D. R. V., B. C.]; Laboratories of Molecular Biophysics, The Rockefeller University, New York, New York 10021 [T. S.]; and Department of Physiology and Biophysics, School of Medicine, State University of New York at Stony Brook, Stony Brook, New York 11794 [W. T. M.]
The inadvertent fusion of the bcr gene with the abl gene results in a constitutively active tyrosine kinase (Bcr-Abl) that transforms cells and causes chronic myelogenous leukemia. Small molecule inhibitors of Bcr-Abl that bind to the kinase domain can be used to treat chronic myelogenous leukemia. We report crystal structures of the kinase domain of Abl in complex with two such inhibitors, imatinib (also known as STI-571 and Gleevec) and PD173955 (Parke-Davis). Both compounds bind to the canonical ATP-binding site of the kinase domain, but they do so in different ways. As shown previously in a crystal structure of Abl bound to a smaller variant of STI-571, STI-571 captures a specific inactive conformation of the activation loop of Abl in which the loop mimics bound peptide substrate. In contrast, PD173955 binds to a conformation of Abl in which the activation loop resembles that of an active kinase. The structure suggests that PD173955 would be insensitive to whether the conformation of the activation loop corresponds to active kinases or to that seen in the STI-571 complex. In vitro kinase assays confirm that this is the case and indicate that PD173955 is at least 10-fold more inhibitory than STI-571. The structures suggest that PD173955 achieves its greater potency over STI-571 by being able to target multiple forms of Abl (active or inactive), whereas STI-571 requires a specific inactive conformation of Abl.
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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||||
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M. Deininger, E. Buchdunger, and B. J. Druker The development of imatinib as a therapeutic agent for chronic myeloid leukemia Blood, April 1, 2005; 105(7): 2640 - 2653. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. R. Burgess, B. J. Skaggs, N. P. Shah, F. Y. Lee, and C. L. Sawyers Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance PNAS, March 1, 2005; 102(9): 3395 - 3400. [Abstract] [Full Text] [PDF] |
||||
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L. J. Elrick, H. G. Jorgensen, J. C. Mountford, and T. L. Holyoake Punish the parent not the progeny Blood, March 1, 2005; 105(5): 1862 - 1866. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. von Bubnoff, D. R. Veach, H. van der Kuip, W. E. Aulitzky, J. Sanger, P. Seipel, W. G. Bornmann, C. Peschel, B. Clarkson, and J. Duyster A cell-based screen for resistance of Bcr-Abl-positive leukemia identifies the mutation pattern for PD166326, an alternative Abl kinase inhibitor Blood, February 15, 2005; 105(4): 1652 - 1659. [Abstract] [Full Text] [PDF] |
||||
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S. Atwell, J. M. Adams, J. Badger, M. D. Buchanan, I. K. Feil, K. J. Froning, X. Gao, J. Hendle, K. Keegan, B. C. Leon, et al. A Novel Mode of Gleevec Binding Is Revealed by the Structure of Spleen Tyrosine Kinase J. Biol. Chem., December 31, 2004; 279(53): 55827 - 55832. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. SAGLIO, A. MOROTTI, G. MATTIOLI, E. MESSA, E. GIUGLIANO, G. VOLPE, G. REGE-CAMBRIN, and D. CILLONI Rational Approaches to the Design of Therapeutics Targeting Molecular Markers: The Case of Chronic Myelogenous Leukemia Ann. N.Y. Acad. Sci., December 1, 2004; 1028(1): 423 - 431. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Wissing, K. Godl, D. Brehmer, S. Blencke, M. Weber, P. Habenberger, M. Stein-Gerlach, A. Missio, M. Cotten, S. Muller, et al. Chemical Proteomic Analysis Reveals Alternative Modes of Action for Pyrido[2,3-d]pyrimidine Kinase Inhibitors Mol. Cell. Proteomics, December 1, 2004; 3(12): 1181 - 1193. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. O'Hare, R. Pollock, E. P. Stoffregen, J. A. Keats, O. M. Abdullah, E. M. Moseson, V. M. Rivera, H. Tang, C. A. Metcalf III, R. S. Bohacek, et al. Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML Blood, October 15, 2004; 104(8): 2532 - 2539. [Abstract] [Full Text] [PDF] |
||||
![]() |
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||||