Perspective of Cyclin-dependent kinase 9 (CDK9) as a Drug Target

被引:113
|
作者
Krystof, Vladimir [1 ,2 ]
Baumli, Sonja [3 ]
Fuerst, Robert [4 ]
机构
[1] Palacky Univ, Lab Growth Regulators, Fac Sci, Olomouc 78371, Czech Republic
[2] Inst Expt Bot ASCR, Olomouc 78371, Czech Republic
[3] Univ Newcastle, No Inst Canc Res, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
[4] Univ Munich, Dept Pharm, Ctr Drug Res Pharmaceut Biol, D-81377 Munich, Germany
基金
英国医学研究理事会;
关键词
Cancer; inflammation; kinase; P-TEFb; inhibitor; therapeutics; angiogenesis; FLAVOPIRIDOL INDUCES APOPTOSIS; GROWTH-FACTOR EXPRESSION; MULTIPLE-MYELOMA CELLS; P-TEFB; TRANSCRIPTION ELONGATION; KAPPA-B; DOWN-REGULATION; CDK9/CYCLIN T1; SELICICLIB CYC202; CRYSTAL-STRUCTURE;
D O I
10.2174/138161212800672750
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Deregulation of cyclin-dependent kinases (CDKs) has been associated with many cancer types and has evoked an interest in chemical inhibitors with possible therapeutic benefit. While most known inhibitors display broad selectivity towards multiple CDKs, recent work highlights CDK9 as the critical target responsible for the anticancer activity of clinically evaluated drugs. In this review, we discuss recent findings provided by structural biologists that may allow further development of highly specific inhibitors of CDK9 towards applications in cancer therapy. We also highlight the role of CDK9 in inflammatory processes and diseases.
引用
收藏
页码:2883 / 2890
页数:8
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