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
. 1996 Aug;134(4):963-70.
doi: 10.1083/jcb.134.4.963.

Role of inhibitory CDC2 phosphorylation in radiation-induced G2 arrest in human cells

P Jin  1 , Y Gu, D O Morgan
Affiliations

Role of inhibitory CDC2 phosphorylation in radiation-induced G2 arrest in human cells

P Jin et al. J Cell Biol. 1996 Aug.

Abstract

The activity of the mitosis-promoting kinase CDC2-cyclin B is normally suppressed in S phase and G2 by inhibitory phosphorylation at Thr14 and Tyr15. This work explores the possibility that these phosphorylations are responsible for the G2 arrest that occurs in human cells after DNA damage. HeLa cell lines were established in which CDC2AF, a mutant that cannot be phosphorylated at Thr14 and Tyr15, was expressed from a tetracycline-repressible promoter. Expression of CDC2AF did not induce mitotic events in cells arrested at the beginning of S phase with DNA synthesis inhibitors, but induced low levels of premature chromatin condensation in cells progressing through S phase and G2. Expression of CDC2AF greatly reduced the G2 delay that resulted when cells were X-irradiated in S phase. However, a significant G2 delay was still observed and was accompanied by high CDC2-associated kinase activity. Expression of wild-type CDC2, or the related kinase CDK2AF, had no effect on the radiation-induced delay. Thus, inhibitory phosphorylation of CDC2, as well as additional undefined mechanisms, delay mitosis after DNA damage.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Bioessays. 1993 Dec;15(12):775-82 - PubMed
    1. Trends Cell Biol. 1994 Jun;4(6):202-7 - PubMed
    1. Nature. 1993 Aug 26;364(6440):824-7 - PubMed
    1. Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5547-51 - PubMed
    1. Cell. 1993 Aug 13;74(3):463-74 - PubMed

Publication types

MeSH terms