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Mutations in PINK1 cause autosomal recessive Parkinson's disease. PINK1 is a mitochondrial kinase of unknown function. We investigated calcium homeostasis and mitochondrial function in PINK1-deficient mammalian neurons. We demonstrate physiologically that PINK1 regulates calcium efflux from the mitochondria via the mitochondrial Na(+)/Ca(2+) exchanger.(More)
Parkinson's disease (PD) is a common age-related neurodegenerative disease and it is critical to develop models which recapitulate the pathogenic process including the effect of the ageing process. Although the pathogenesis of sporadic PD is unknown, the identification of the mendelian genetic factor PINK1 has provided new mechanistic insights. In order to(More)
Recent experiments show that the microtubule-associated protein (MAP) 1B is a major phosphorylation substrate for the serine/threonine kinase glycogen synthase kinase-3beta (GSK-3beta) in differentiating neurons. GSK-3beta phosphorylation of MAP1B appears to act as a molecular switch regulating the control that MAP1B exerts on microtubule dynamics in(More)
The serine/threonine kinase glycogen synthase kinase-3beta (GSK-3beta) is expressed in two, alternatively spliced, isoforms: a short form (GSK-3beta1) and a long form containing a 13 amino acid insert in the catalytic domain (GSK-3beta2). We examined the expression of these isoforms in the rat using specific antibodies and found that GSK-3beta2, in contrast(More)
Mitochondrial Na(+)/Ca(2+) exchange (NCXmito) is critical for neuronal Ca(2+) homeostasis and prevention of cell death from excessive mitochondrial Ca(2+) (m[Ca(2+)]) accumulation. The mitochondrial kinase PINK1 appears to regulate the mCa(2+) efflux from dopaminergic (DAergic) neurons, possibly by directly regulating NCXmito. However, the precise molecular(More)
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