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Biology Direct

, 12:6

Cell Biology

AbstractMutations in the gene encoding for the E3 ubiquitin ligase Parkin are associated to a rare form of familiar autosomal recessive Parkinsonism. Despite decades of research on the Parkin protein, whose structure has been recently solved, little is known about the specific signalling pathways that lead to Parkin activation. Parkin activity spans from mitochondria quality control to tumor suppression and stress protection; it is thus tempting to hypothesize that the broad impact of Parkin on cellular physiology might be the result of different post translational modifications that can be controlled by balanced opposing events. Sequence alignment of Parkin from different species indicates high homology between domains across Parkin orthologs and identifies highly conserved amino acid residues that, if modified, impinge on Parkin functions. In this review, we summarize findings on post translational modifications that have been shown to affect Parkin activity and stability.

ReviewersThis article was reviewed by Prof. Dr. Konstanze F. Winklhofer and by Prof. Thomas Simmen. Both reviewers have been nominated by Professor Luca Pellegrini.

KeywordsParkinson’s disease Parkin Post translational modifications Ubiquitination Phosphorylation AbbreviationsCdk-5Cyclin dependent kinase 5

Ck-1Casein kinase 1

DUBsDeubiquitination enzymes

H2SHydrogen sulphide

IBRIn between RING finger domain

NONitric oxide

OMMOuter mitochondrial membrane

PDParkinson’s Disease

REPRepressive element of Parkin

SUMOSmall ubiquitin like modifiers

UPSUbiquitin-proteasome system

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Autor: Joy Chakraborty - Valentina Basso - Elena Ziviani


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