Impaired genomic stability and increased oxidative stress exacerbate different features of Ataxia-telangiectasia-Reference-Cited by-同舟云学术

Impaired genomic stability and increased oxidative stress exacerbate different features of Ataxia-telangiectasia

Published:2005-09-08 Issue:19 Volume:14 Page:2929-2943
ISSN:1460-2083
Container-title:Human Molecular Genetics
language:en
Short-container-title:

Author:

Ziv Shelly,Brenner Ori,Amariglio Ninette,Smorodinsky Nechama I.,Galron Ronit,Carrion Danaise V.,Zhang Weijia,Sharma Girdhar G.,Pandita Raj K.,Agarwal Manjula,Elkon Ran,Katzin Nirit,Bar-Am Irit,Pandita Tej K.,Kucherlapati Raju,Rechavi Gideon,Shiloh Yosef,Barzilai Ari

Publisher

Oxford University Press (OUP)

Subject

Genetics (clinical),Genetics,Molecular Biology,General Medicine

Link

http://academic.oup.com/hmg/article-pdf/14/19/2929/17241692/ddi324.pdf

Reference44 articles.

1. Chun, H.H. and Gatti, R.A. (2004) Ataxia-telangiectasia, an evolving phenotype. DNA Repair (Amst), 3, 1187–1196.

2. Abraham, R.T. (2004) PI 3-kinase related kinases: ‘big’ players in stress-induced signaling pathways. DNA Repair (Amst), 3, 883–887.

3. Shiloh, Y. (2003) ATM and related protein kinases: safeguarding genome integrity. Nat. Rev. Cancer, 3, 155–168.

4. Bakkenist, C.J. and Kastan, M.B. (2003) DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation. Nature, 421, 499–506.

5. Kurz, E.U. and Lees-Miller, S.P. (2004) DNA damage-induced activation of ATM and ATM-dependent signaling pathways. DNA Repair (Amst), 3, 889–900.

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