Structure-Functional Prediction and Analysis of Cancer Mutation Effects in Protein Kinases

被引:29
作者
Dixit, Anshuman [1 ,2 ]
Verkhivker, Gennady M. [3 ,4 ,5 ]
机构
[1] Univ Kansas, Sch Pharm, Dept Pharmaceut Chem, Lawrence, KS 66047 USA
[2] Inst Life Sci, Dept Biotechnol, Bhubaneswar, Orissa, India
[3] Chapman Univ, Sch Computat Sci, Schmid Coll Sci & Technol, Orange, CA 92866 USA
[4] Chapman Univ, Crean Sch Hlth & Life Sci, Schmid Coll Sci & Technol, Orange, CA 92866 USA
[5] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA
关键词
GROWTH-FACTOR RECEPTOR; OF-FUNCTION MUTATIONS; ABL TYROSINE KINASE; EGF RECEPTOR; LUNG-CANCER; COLORECTAL CANCERS; MOLECULAR-DYNAMICS; SOMATIC MUTATIONS; CRYSTAL-STRUCTURES; HUMAN BREAST;
D O I
10.1155/2014/653487
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
A central goal of cancer research is to discover and characterize the functional effects of mutated genes that contribute to tumorigenesis. In this study, we provide a detailed structural classification and analysis of functional dynamics for members of protein kinase families that are known to harbor cancer mutations. We also present a systematic computational analysis that combines sequence and structure-based prediction models to characterize the effect of cancer mutations in protein kinases. We focus on the differential effects of activating point mutations that increase protein kinase activity and kinase-inactivating mutations that decrease activity. Mapping of cancer mutations onto the conformational mobility profiles of known crystal structures demonstrated that activating mutations could reduce a steric barrier for the movement from the basal "low" activity state to the "active" state. According to our analysis, the mechanism of activating mutations reflects a combined effect of partial destabilization of the kinase in its inactive state and a concomitant stabilization of its active-like form, which is likely to drive tumorigenesis at some level. Ultimately, the analysis of the evolutionary and structural features of the major cancer-causing mutational hotspot in kinases can also aid in the correlation of kinase mutation effects with clinical outcomes.
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页数:24
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共 136 条
[1]   Structural Analysis of the Mechanism of Inhibition and Allosteric Activation of the Kinase Domain of HER2 Protein [J].
Aertgeerts, Kathleen ;
Skene, Robert ;
Yano, Jason ;
Sang, Bi-Ching ;
Zou, Hua ;
Snell, Gyorgy ;
Jennings, Andy ;
Iwamoto, Keiji ;
Habuka, Noriyuki ;
Hirokawa, Aki ;
Ishikawa, Tomoyasu ;
Tanaka, Toshimasa ;
Miki, Hiroshi ;
Ohta, Yoshikazu ;
Sogabe, Satoshi .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (21) :18756-18765
[2]   Map2k4 Functions as a Tumor Suppressor in Lung Adenocarcinoma and Inhibits Tumor Cell Invasion by Decreasing Peroxisome Proliferator-Activated Receptor γ2 Expression [J].
Ahn, Young-Ho ;
Yang, Yanan ;
Gibbons, Don L. ;
Creighton, Chad J. ;
Yang, Fei ;
Wistuba, Ignacio I. ;
Lin, Wei ;
Thilaganathan, Nishan ;
Alvarez, Cristina A. ;
Roybal, Jonathon ;
Goldsmith, Elizabeth J. ;
Tournier, Cathy ;
Kurie, Jonathan M. .
MOLECULAR AND CELLULAR BIOLOGY, 2011, 31 (21) :4270-4285
[3]  
Amadei A, 1999, PROTEINS, V36, P419, DOI 10.1002/(SICI)1097-0134(19990901)36:4<419::AID-PROT5>3.0.CO
[4]  
2-U
[5]   ESSENTIAL DYNAMICS OF PROTEINS [J].
AMADEI, A ;
LINSSEN, ABM ;
BERENDSEN, HJC .
PROTEINS-STRUCTURE FUNCTION AND GENETICS, 1993, 17 (04) :412-425
[6]   T-Cell Signaling Regulated by the Tec Family Kinase, Itk [J].
Andreotti, Amy H. ;
Schwartzberg, Pamela L. ;
Joseph, Raji E. ;
Berg, Leslie J. .
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY, 2010, 2 (07) :a002287
[7]   Architecture and Membrane Interactions of the EGF Receptor [J].
Arkhipov, Anton ;
Shan, Yibing ;
Das, Rahul ;
Endres, Nicholas F. ;
Eastwood, Michael P. ;
Wemmer, David E. ;
Kuriyan, John ;
Shaw, David E. .
CELL, 2013, 152 (03) :557-569
[8]   A novel mode of Gleevec binding is revealed by the structure of spleen tyrosine kinase [J].
Atwell, S ;
Adams, JM ;
Badger, J ;
Buchanan, MD ;
Feil, IK ;
Froning, KJ ;
Gao, X ;
Hendle, J ;
Keegan, K ;
Leon, BC ;
Müller-Dieckmann, HJ ;
Nienaber, VL ;
Noland, BW ;
Post, K ;
Rajashankar, KR ;
Ramos, A ;
Russell, M ;
Burley, SK ;
Buchanan, SG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (53) :55827-55832
[9]   Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL [J].
Azam, M ;
Latek, RR ;
Daley, GQ .
CELL, 2003, 112 (06) :831-843
[10]   Asymmetric tyrosine kinase arrangements in activation or autophosphorylation of receptor tyrosine kinases [J].
Bae, Jae Hyun ;
Schlessinger, Joseph .
MOLECULES AND CELLS, 2010, 29 (05) :443-448