Evidence map›Paper›PMID 30081712›Full record

ArticleAutophagy2018

MFN2 retrotranslocation boosts mitophagy by uncoupling mitochondria from the ER.

Gian-Luca McLelland, Edward A Fon

Abstract readComment
In one paragraph

Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Gian-Luca McLellanda McGill Parkinson Program and Neurodegenerative Diseases Group, Montreal Neurological Institute and Department of Neurology and Neurosurgery , McGill University , Montreal , Canada.ORCID 0000-0002-6122-6252
Edward A Fona McGill Parkinson Program and Neurodegenerative Diseases Group, Montreal Neurological Institute and Department of Neurology and Neurosurgery , McGill University , Montreal , Canada.ORCID 0000-0002-5520-6239

Funding

CIHR
6 · The paper itself

Abstract

Mitochondrial damage triggers mitochondrial quality control pathways, which act to ensure the health of the mitochondrial network. The turnover of damaged mitochondria by mitophagy is initiated by the Parkinson disease-linked genes PRKN and PINK1, and we recently investigated the role that interorganellar contact sites between the endoplasmic reticulum (ER) and the outer mitochondrial membrane (OMM) play in this pathway. In this punctum, we summarize our findings that show that the ER-OMM tether MFN2 acts as a suppressor of mitophagy through its ability to link the OMM to the ER, potentially limiting the accessibility of other ubiquitination substrates to PINK1 and PRKN. PINK1, PRKN and the AAA-ATPase VCP disrupt contact between mitochondria and the ER via MFN2 ubiquitination, retrotranslocation and turnover from the mitochondrial membrane. Our study provides insight into the role of OMM remodeling in mitophagy.

Indexed as

AutophagyMitophagyMitochondriaProtein KinasesUbiquitinationUbiquitin-Protein LigasesProtein KinasesUbiquitin-Protein LigasesContact siteMFN2mitophagyParkinson’s diseasephosphoubiquitinPINK1-PRKN pathway

Identifiers

PMID30081712
PMCPMC6135574

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.