4.8 Editorial Material

How could Parkin-mediated ubiquitination of mitofusin promote mitophagy?

期刊

AUTOPHAGY
卷 6, 期 5, 页码 660-662

出版社

LANDES BIOSCIENCE
DOI: 10.4161/auto.6.5.12242

关键词

Parkinson disease; neurodegeneration; Parkin; PINK1; Mfn; mitochondrial dynamics; ubiquitination; Drosophila

资金

  1. Medical Research Council [MC_G1000735] Funding Source: Medline
  2. Wellcome Trust [089698] Funding Source: Medline
  3. Medical Research Council [MC_G1000735] Funding Source: researchfish
  4. MRC [MC_G1000735] Funding Source: UKRI

向作者/读者索取更多资源

Much evidence links mitochondrial dysfunction to the death of neurons in Parkinson disease (PD), and is particularly emphasized by our growing understanding of the function of genes linked to recessively inherited PD such as PINK1, parkin and DJ-1. Recent work has revealed an exciting link between the PINK1-Parkin pathway and the autophagic turnover of dysfunctional mitochondrial (mitophagy). We have recently shown that mitofusin is ubiquitinated by Parkin when it is recruited to dysfunctional mitochondria. Recent work also shows that regulated fission and fusion events help segregate dysfunctional mitochondria prior to mitophagy. Here we hypothesize how Parkin-mediated ubiquitination of Mfn may play a role in this mechanism.

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