IMR Press / FBL / Volume 11 / Issue 3 / DOI: 10.2741/1994

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article
Mechanisms controlling CDK9 activity
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1 Fels Institute for Cancer Research and Molecular Biology and Department of Biochemistry. Temple University School of Medicine. 3307 North Broad St., Philadelphia, PA 19140, USA
Front. Biosci. (Landmark Ed) 2006, 11(3), 2598–2613; https://doi.org/10.2741/1994
Published: 1 September 2006
Abstract

This review primarily focuses on the mechanisms that modulate CDK9 activity and its recruitment to cellular genes, where it phosphorylates the C-terminal domain of RNA polymerase II (RNAPII) as well as negative elongation factors. CDK9 associates with each of four cyclins (T1, T2a, T2b and K), forming distinct positive transcription elongation factors (P-TEFb). Research done during the past decade has demonstrated a role for P-TEFb in stimulating elongation of otherwise paused RNAPII transcripts. Recent work suggests that P-TEFb also positively modulates other steps during transcription. In addition, "abnormal" CDK9 function is associated with certain diseases. Specifically, the activity of the cyclin T1/CDK9 complex is essential for HIV-1 replication and CDK9 upregulation is associated with cardiac hypertrophy. Thus, the role of CDK9 in these processes, and the possibility of therapeutically targeting CDK9, will also be briefly discussed.

Keywords
CDK9
CDK7
CDK
Cyclin T1
Cyclin T2a
cyclin T2b
RNA Polymerase II
transcription
Kinase
HIV Tat
Hexim
Brd4
7 small nuclear RNA
RNA polymerase II CTD
CDK inhibitors
Review
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