Atm‐null mice exhibit enhanced radiation‐induced birth defects and a hybrid form of embryonic cell death indicating a teratological suppressor function for ATM-Reference-Cited by-同舟云学术

Atm‐null mice exhibit enhanced radiation‐induced birth defects and a hybrid form of embryonic cell death indicating a teratological suppressor function for ATM

Published:2004-03-19 Issue:7 Volume:18 Page:896-898
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Laposa Rebecca R.¹,Henderson Jeffrey T.¹,Xu Elaine¹,Wells Peter G.¹²

Affiliation:

1. Faculty of PharmacyUniversity of TorontoTorontoCanada

2. Department of PharmacologyUniversity of TorontoTorontoCanada

Funder

Canadian Institutes of Health Research

Society of Toxicology

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.03-0903fje

Reference44 articles.

1. Multiple ATM-Dependent Pathways: An Explanation for Pleiotropy

2. Hypothesis: Ataxia-telangiectasia: Is ATM a sensor of oxidative damage and stress?

3. The Product of the ATM Gene Is a 370-kDa Nuclear Phosphoprotein

4. Atm expression patterns suggest a contribution from the peripheral nervous system to the phenotype of ataxia–telangiectasia

5. Ataxia‐telangiectasia and cellular responses to DNA damage;Meyn M. S.;Cancer Res.,1995

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