Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 19 November 2002
Vol. 2002, Issue 159, p. tw434
[DOI: 10.1126/stke.2002.159.tw434]

EDITORS' CHOICE

CELL CYCLE Surveying the Damage

Normal cells respond to DNA damage by halting the cell cycle and initiating DNA repair, thereby preventing accumulation of potentially serious genetic abnormalities. Several proteins are important in controlling DNA damage checkpoints, but details about how they cooperate have yet to be worked out. Wang et al. focused their attention on 53BP1, a protein originally identified through its ability to bind the tumor suppressor protein p53. Inhibition of 53BP1 with small interfering RNA (siRNA) prevented the reduction in DNA synthesis and cell-cycle progression normally seen after exposure of cells to moderate levels of ionizing radiation. This change corresponded with a partial decrease in phosphorylation of other checkpoint proteins, Brca1 and Chk2, by 53BP1 and the disruption of Brca1 foci formation within the nucleus in response to ionizing radiation. 53BP1 therefore appears to play a direct role in preserving genomic stability through the regulation of checkpoint control signals and DNA repair machinery.

B. Wang, S. Matsuoka, P. B. Carpenter, S. J. Elledge, 53BP1, a mediator of the DNA damage checkpoint. Science 298, 1435-1438 (2002). [Abstract] [Full Text]

Citation: Surveying the Damage. Sci. STKE 2002, tw434 (2002).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882