IMR Press / FBL / Volume 5 / Issue 3 / DOI: 10.2741/bregman

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 as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Cell cycle regulation and RNA polymerase II
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1 Dept. of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
2 Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
3 Dept. of Tumor Cell Biology, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105, USA
Academic Editor:Richard Pestell
Front. Biosci. (Landmark Ed) 2000, 5(3), 244–257;
Published: 1 February 2000
(This article belongs to the Special Issue Cell cycle dysregulation in disease)

The cell cycle and transcription by RNA polymerase II (RNAP II) are closely related. They utilize shared components. RNAP II transcriptional activity is modulated during the cell cycle. Cell cycle dependent changes in the phosphorylation status of the carboxyl-terminal domain (CTD) of the largest subunit of RNAP II (RNAP II-LS) alter transcription. Several CTD kinases are members of the cyclin-dependent kinase (cdk) superfamily, including p34cdc2 (cdk1), cdk7, cdk8, and cdk9. Each of these cdks, with their respective cyclin partners, have been linked to cell cycle regulatory events. Other CTD kinases such as casein kinase II (CKII) and c-abl have also been implicated in cell cycle dependent modifications of the CTD. In addition, the stalling of RNAP II complexes at DNA lesions helps stimulate p53 accumulation which largely determines the cell's DNA damage response, including cell cycle arrest. Alzheimer's disease pathology results partially from activation of mitotic cdks in postmitotic neurons which can phosphorylate RNAP II-LS and other targets.

Cell cycle
RNA polymerase II
Cyclin dependent kinase
Alzheimer’s disease
Cockayne syndrome
DNA damage
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