Article
Atm-null mice exhibit enhanced radiation-induced birth defects and a hybrid form of embryonic programmed cell death indicating a teratological suppressor function for ATM.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology - 1 May 2004
Laposa Rebecca R, Henderson Jeffrey T, Xu Elaine, Wells Peter G
Abstract excerpt
ATM (ataxia-telangiectasia mutated) is a genotoxic stress transducer. In this first report of Atm-dependent birth defects, Atm-null embryos were uniquely susceptible to low-dose (0.5 Gy) radiation, exhibiting severe runting, tail anomalies, and lethality, independent of cell cycle arrest or insul...
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