Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017:953:83-116.
doi: 10.1007/978-3-319-46095-6_3.

Regulation of Cell Division

Affiliations
Review

Regulation of Cell Division

Andreas Heim et al. Adv Exp Med Biol. 2017.

Erratum in

  • Erratum.
    Pelegri F, Danilchik M, Sutherland A. Pelegri F, et al. Adv Exp Med Biol. 2017;953:E1. doi: 10.1007/978-3-319-46095-6_11. Adv Exp Med Biol. 2017. PMID: 28299712 No abstract available.

Abstract

The challenging task of mitotic cell divisions is to generate two genetically identical daughter cells from a single precursor cell. To accomplish this task, a complex regulatory network evolved, which ensures that all events critical for the duplication of cellular contents and their subsequent segregation occur in the correct order, at specific intervals and with the highest possible fidelity. Transitions between cell cycle stages are triggered by changes in the phosphorylation state and levels of components of the cell cycle machinery. Entry into S-phase and M-phase are mediated by cyclin-dependent kinases (Cdks), serine-threonine kinases that require a regulatory cyclin subunit for their activity. Resetting the system to the interphase state is mediated by protein phosphatases (PPs) that counteract Cdks by dephosphorylating their substrates. To avoid futile cycles of phosphorylation and dephosphorylation, Cdks and PPs must be regulated in a manner such that their activities are mutually exclusive.

Keywords: Anaphase-promoting complex/cyclosome (APC/C); Cell cycle regulation; Cyclin-dependent kinase 1 (Cdk1); Type 1 protein phosphatase (PP1); Type 2A protein phosphatase (PP2A).

PubMed Disclaimer

Similar articles

Cited by

Publication types

Substances

LinkOut - more resources