A Developmental Role for Ataxia-Telangiectasia Mutated in Protecting the Embryo from Spontaneous and Phenytoin-Enhanced Embryopathies in Culture
Author:
Publisher
Oxford University Press (OUP)
Subject
Toxicology
Link
http://academic.oup.com/toxsci/article-pdf/93/1/156/10954218/kfl045.pdf
Reference33 articles.
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3. Barlow, C., Ribaut-Barasin, C., Zwingman, T. A., Pope, A. J., Brown, K. D., Owens, J. W., Larson, D., Harrington, E. A., Haeberle, A. M., Mariani, J., et al. (2000). ATM is a cytosolic protein in mouse brain required to prevent lysosomal accumulation. Proc. Natl. Acad. Sci. U.S.A.97,871–876.
4. Bhuller, Y., Jeng, W., and Wells, P. G. (2006). Variable in vivo embryoprotective role for ataxia telangiectasia-mutated (Atm) against constitutive and phenytoin-enhanced oxidative stress in Atm knockout mice. Toxicol. Sci. 93,146–155.
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