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Pharmacological targeting of CDK9 in cardiac hypertrophy
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SYSNO ASEP 0359307 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Pharmacological targeting of CDK9 in cardiac hypertrophy Author(s) Kryštof, Vladimír (UEB-Q) RID, ORCID
Chamrád, Ivo (UEB-Q) ORCID
Jorda, Radek (UEB-Q) ORCID, RID
Kohoutek, J. (CZ)Number of authors 4 Source Title Medicinal Research Reviews. - : Wiley - ISSN 0198-6325
Roč. 30, č. 4 (2010), s. 646-666Number of pages 21 s. Language eng - English Country US - United States Keywords P-TEFb ; cardiac myocyte ; cardiac hypertrophy Subject RIV CE - Biochemistry R&D Projects GA204/08/0511 GA ČR - Czech Science Foundation (CSF) GA301/09/1832 GA ČR - Czech Science Foundation (CSF) GA301/08/1649 GA ČR - Czech Science Foundation (CSF) CEZ AV0Z50380511 - UEB-Q (2005-2011) UT WOS 000278760700003 DOI 10.1002/med.20172 Annotation Cardiac hypertrophy allows the heart to adapt to workload, but persistent or unphysiological stimulus can result in pump failure. Cardiac hypertrophy is characterized by an increase in the size of differentiated cardiac myocytes. At the molecular level, growth of cells is linked to intensive transcription and translation. Several cyclin-dependent kinases (CDKs) have been identified as principal regulators of transcription, and among these CDK9 is directly associated with cardiac hypertrophy. CDK9 phosphorylates the C-terminal domain of RNA polymerase II and thus stimulates the elongation phase of transcription. Chronic activation of CDK9 causes not only cardiac myocyte enlargement but also confers predisposition to heart failure. Due to the long interest of molecular oncologists and medicinal chemists in CDKs as potential targets of anticancer drugs, a portfolio of small-molecule inhibitors of CDK9 is available. Workplace Institute of Experimental Botany Contact David Klier, knihovna@ueb.cas.cz, Tel.: 220 390 469 Year of Publishing 2012
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