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, 6 April 2004
Vol. 2004, Issue 227, p. tw128
[DOI: 10.1126/stke.2272004tw128]

EDITORS' CHOICE

CHECKPOINTS Complex Response to DNA Damage

Cells avoid the disastrous effects of DNA damage by activating a checkpoint mechanism to prevent proliferation of cells that contain damaged DNA. The protein kinase ATM is an important component of this signaling mechanism, but precisely how its activity is regulated has not been clear. The protein Nbs1, which is mutated in the human disorder Nijmegen breakage syndrome, forms MRN complexes with two other proteins that participate in DNA repair, Mre11 and Rad50 (Mre11-Rad50-Nbs1, hence, MRN). Nbs is also a substrate for ATM. But now, Lee and Paull suggest that the interaction between Nbs1 and ATM is more complicated. MRN complexes directly activate enzymatic activity of ATM, possibly by causing a conformational change in ATM that alters the affinity of the kinase toward its substrates.

J.-H. Lee, T. T. Paull, Direct activation of the ATM protein kinase by the Mre11/Rad50/Nbs1 complex. Science 304, 93-96 (2004). [Abstract] [Full Text]

Citation: Complex Response to DNA Damage. Sci. STKE 2004, tw128 (2004).


To Advertise     Find Products


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