DJ-1 function and oxidative stress
$182,454ZIAFY2016AGNIH
National Institute On Aging
Investigators
Linked publications & trials
Paper 35713360Paper 34196120Paper 28962651Paper 27659605Paper 26965687Paper 24832775Paper 24722488Paper 22951446Paper 21413989Paper 21317550Paper 20940149Paper 20696314Paper 20187230Paper 19146923Paper 19124468Paper 17590087Paper 17394548Paper 17182998Paper 17068789Paper 16750377Paper 16687141Paper 16364891Paper 16280683Paper 15955416Paper 15952880Paper 15824318Paper 15790532Paper 15773923Paper 15663963Paper 15663960Paper 15547643Paper 15306116Paper 15294138Paper 15181200Paper 15180968Paper 15159488Paper 15070401Paper 14987449Paper 14662519Paper 14593171Paper 14509657Paper 12886009Paper 12851414Paper 12849210Paper 12842030Paper 12749984Paper 12716427Paper 12526767Paper 12475980Paper 12358759Paper 12215229Paper 12177198Paper 12165567Paper 12098639Paper 12077002Paper 11958831Paper 11290408Paper 10800932
Abstract
We have been interested in the relationship between oxidative stress and DJ-1, a rare cause of recessive Parkinson's disease, for several years and have focussed the relationship between oxidative stress and mitochondrial localization. In the current period, we have explored the effects of DJ-1 deficiency in the brains of mice and rats. We find that loss of DJ-1 alters cellular signaling pathways that result, at a cellular level, in the accumulation of changes in metabolic enyzmes. We are currently exploring the mechanism(s) by which this occurs and determining the output of these changes on neurons and glia in the brain.
View original record on NIH RePORTER →