Journal
FEBS JOURNAL
Volume 275, Issue 23, Pages 5758-5766Publisher
WILEY
DOI: 10.1111/j.1742-4658.2008.06708.x
Keywords
cell death; DJ-1; HtrA2; mitochondria; mutation; neuron; Parkin; Parkinson's disease; PINK1; signalling
Categories
Funding
- Medical Research Council [G0700183] Funding Source: Medline
- MRC [G0700183] Funding Source: UKRI
- Medical Research Council [G0700183] Funding Source: researchfish
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available