Characterising the effects of oxidative stress on the human L-type Ca2+ channel isoforms and role in human pathology

Funding Activity

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Funded Activity Summary

Oxidative stress, poor energy production and increases in intracellular calcium are features of the failing heart. I have determined that the function of the L-type calcium channel, the primary protein responsible for calcium influx and contraction can be regulated by free radicals produced by the mitochondria (powerhouse of the cell). This proposal will determine the site of modification on the human L-type calcium channel and how communication between the channel and the mitochondria is altered in animal models of human disease.

Funded Activity Details

Start Date: 01-01-2011

End Date: 01-01-2016

Funding Scheme: Research Fellowships

Funding Amount: $250,805.00

Funder: National Health and Medical Research Council

Research Topics

ANZSRC Field of Research (FoR)

Cardiology (incl. Cardiovascular Diseases)

ANZSRC Socio-Economic Objective (SEO)

There are no SEO codes available for this funding activity

Other Keywords

Aboriginal health | calcium | calcium channels | cardiac disease | cardiac hypertrophy | mitochondria | oxidative stress | prevention