The appropriateness of the mouse model for ataxia-telangiectasia: Neurological defects but no neurodegeneration-Reference-Cited by-同舟云学术

The appropriateness of the mouse model for ataxia-telangiectasia: Neurological defects but no neurodegeneration

Published:2013-08 Issue:8 Volume:12 Page:612-619
ISSN:1568-7864
Container-title:DNA Repair
language:en
Short-container-title:DNA Repair

Author:

Lavin Martin F.

Funder

Australian National Health and Medical Research Council

A-T Children's Project

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference83 articles.

1. Ataxia-telangiectasia, A familial syndrome of progressive cerebellar ataxia, oculocutaneous telangiectasia and frequent pulmonary infection. A preliminary report on 7 children, an autopsy, and a case history;Boder;Univ. South. Calif. Med. Bull.,1957

2. Localization of an ataxia-telangiectasia gene to chromosome 11q22-23;Gatti;Nature,1988

3. A single ataxia telangiectasia gene with a product similar to PI-3 kinase;Savitsky;Science,1995

4. Ataxia-telangiectasia;Sedgwick,1991

5. Ataxia-telangiectasia: an overview;Boder;Kroc Found. Ser.,1985

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