Role of oxidative stress in activating ATM to protect against neurodegeneration

Funding Activity

Website
http://purl.org/au-research/grants/nhmrc/1019996

Funding Status
Closed

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Funded Activity Summary

ATM is the protein defective in the human genetic disorder ataxia-telangiectasia (A-T). This project is designed to investigate how this protein is activated by oxidative stress. The study is largely a mechanistic one, to investigate changes occurring in ATM as part of the activation process. There is evidence that ATM exists in the cytoplasm in neuronal cells and understanding its function in these cells may assist in understanding the basis for neurodegeneration in A-T.

Funded Activity Details

Start Date: 01-01-2012

End Date: 01-01-2014

Funding Scheme: Project Grants

Funding Amount: $570,334.00

Funder: National Health and Medical Research Council

Research Topics

ANZSRC Field of Research (FoR)

Signal Transduction

ANZSRC Socio-Economic Objective (SEO)

There are no SEO codes available for this funding activity

Other Keywords

DNA damage | ataxia telangiectasia | genetics | neuronal degeneration | oxidative stress | phosphorylation | signal transduction

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