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

被引:28
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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