Article
Impaired genomic stability and increased oxidative stress exacerbate different features of Ataxia-telangiectasia.
Human molecular genetics - 1 Oct 2005
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
Abstract excerpt
Ataxia-telangiectasia (A-T) is a multisystem, cancer-predisposing genetic disorder caused by deficiency of the ATM protein. To dissect the A-T phenotype, we augmented specific features of the human disease by generating mouse strains that combine Atm deficiency with dysfunction of other proteins. Increasing oxidative stress by combining deficiencies in Atm and superoxide dismutase 1 (Sod1) exacerbated growth...
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