ATM signaling and genornic stability in response to DNA damage


Autoria(s): Lavin, Martin F.; Birrell, Geoff; Chen, Philip; Kozlov, Sergei; Scott, Shaun; Gueven, Nuri
Contribuinte(s)

P. J. Stambrook

L. H. F. Mullenders

L. R. Ferguson

Data(s)

01/01/2005

Resumo

DNA double strand breaks represent the most threatening lesion to the integrity of the genome in cells exposed to ionizing radiation and radiomimetic chemicals. Those breaks are recognized, signaled to cell cycle checkpoints and repaired by protein complexes. The product of the gene (ATM) mutated in the human genetic disorder ataxia-telangietasia (A-T) plays a central role in the recognition and signaling of DNA damage. ATM is one of an ever growing number of proteins which when mutated compromise the stability of the genome and predispose to tumour development. for recognising double strand breaks in DNA, maintaining genome stability and minimizing risk of cancer are discussed. (C) 2004 Published by Elsevier B.V.

Identificador

http://espace.library.uq.edu.au/view/UQ:76393

Idioma(s)

eng

Publicador

Elsevier Science Bv

Palavras-Chave #Atm Signaling #Genomic Stability #Ataxia-telangiectasia #Biotechnology & Applied Microbiology #Genetics & Heredity #Toxicology #Double-strand Breaks #Ataxia-telangiectasia Heterozygotes #S-phase Checkpoint #Cell-cycle #Homologous Recombination #Saccharomyces-cerevisiae #Mre11 Phosphorylation #Ionizing-radiation #Genomic Instability #Missense Mutations #C1 #270103 Protein Targeting and Signal Transduction #730107 Inherited diseases (incl. gene therapy)
Tipo

Journal Article