[go: up one dir, main page]
Wikipedia

Parkin (protein): Difference between revisions

Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
m →‎Parkinson’s Disease: Journal cites, Added 1 doi to a journal cite
No edit summary
Line 1:
{{other uses|Parkin (disambiguation)}}
{{Infobox_gene}}
Parkin is ana 465-[[residue (chemistry)|residue]] E3 [[ubiquitin ligase]] that plays a critical role in [[ubiquitination]]- the process whereby molecules are covalently labelled with [[ubiquitin]] (Ub) and directed towards degradation in [[proteasomes]] or [[lysosomes]]. Ubiquitination involves the sequential action of three enzymes. Firstly, an E1 [[ubiquitin-activating enzyme]] binds to inactive Ub in [[eukaryotic cells]] via a [[thioester]] bond and mobilises it in an ATP-dependent process. Ub is then transferred to an E2 [[ubiquitin-conjugating enzyme]] before being conjugated to the target protein via an E3 [[ubiquitin ligase]].<ref name="Pickart and Eddins 2004">{{cite journal | vauthors = Pickart CM, Eddins MJ | title = Ubiquitin: structures, functions, mechanisms | journal = Biochimica et Biophysica Acta | volume = 1695 | issue = 1–3 | pages = 55–72 | date = November 2004 | pmid = 15571809 | doi = 10.1016/j.bbamcr.2004.09.019 }}</ref> There exists a multitude of E3 ligases, which differ in structure and substrate specificity to allow selective targeting of proteins to intracellular degradation.
 
In particular, parkin recognises proteins on the outer membrane of [[mitochondria]] upon cellular insult and mediates the clearance of damaged mitochondria via [[autophagy]] and proteasomal mechanisms.<ref name="Seirafi_2015">{{cite journal | vauthors = Seirafi M, Kozlov G, Gehring K | title = Parkin structure and function | journal = The FEBS Journal | volume = 282 | issue = 11 | pages = 2076–88 | date = June 2015 | pmid = 25712550 | pmc = 4672691 | doi = 10.1111/febs.13249 }}</ref> Parkin also enhances cell survival by suppressing both mitochondria-dependent and -independent [[apoptosis]]. [[Mutations]] are associated with mitochondrial dysfunction, leading to neuronal death in [[Parkinson’s disease]]<ref name="Dawson 2014">{{cite journal | vauthors = Dawson TM, Dawson VL | title = The role of parkin in familial and sporadic Parkinson's disease | journal = Movement Disorders | volume = 25 | issue = Suppl 1 | pages = S32-9 | date = 2014 | pmid = 20187240 | doi = 10.1002/mds.22798 | pmc=4115293}}</ref> and aberrant [[metabolism]] in [[tumourigenesis]].<ref name="Zhang 2011">{{cite journal | vauthors = Zhang C, Lin M, Wu R, Wang X, Yang B, Levine AJ, Hu W, Feng Z | title = Parkin, a p53 target gene, mediates the role of p53 in glucose metabolism and the Warburg effect | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 108 | issue = 39 | pages = 16259–64 | year = 2011 | pmid = 21930938 | pmc = 3182683 | doi = 10.1073/pnas.1113884108 }}</ref>
Retrieved from "https://en.wikipedia.org/wiki/Parkin_(protein)"