期刊
FEBS JOURNAL
卷 275, 期 23, 页码 5758-5766出版社
WILEY
DOI: 10.1111/j.1742-4658.2008.06708.x
关键词
cell death; DJ-1; HtrA2; mitochondria; mutation; neuron; Parkin; Parkinson's disease; PINK1; signalling
资金
- Medical Research Council [G0700183] Funding Source: Medline
- MRC [G0700183] Funding Source: UKRI
- Medical Research Council [G0700183] Funding Source: researchfish
Rare, inherited mutations causing familial forms of Parkinson's disease have provided insight into the molecular mechanisms that underlie the genetic and sporadic forms of this disease. Loss of protein function resulting from autosomal-recessive mutations in PTEN-induced putative kinase 1 (PINK1), Parkin and DJ-1 has been linked to mitochondrial dysfunction, accumulation of abnormal and misfolded proteins, impaired protein clearance and oxidative stress. Accumulating evidence suggests that wild-type PINK1, Parkin and DJ-1 may be key components of neuroprotective signalling cascades that run in parallel, interact via cross talk or converge in a common pathway.
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