Evidence map›Paper›PMID 30058425›Full record

ArticleAutophagy2018

Actin cages isolate damaged mitochondria during mitophagy.

Antonina J Kruppa, Folma Buss

Open access · bronzeAbstract 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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Deciphering the Role of Selenoprotein M.Antioxidants (Basel, Switzerland) · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Mitophagy and Neurodegeneration: Between the Knowns and the Unknowns.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Antonina J Kruppaa Department of Clinical Biochemistry , Cambridge Institute for Medical Research, University of Cambridge , Cambridge , UK.
Folma Bussa Department of Clinical Biochemistry , Cambridge Institute for Medical Research, University of Cambridge , Cambridge , UK.
University of Cambridge · GB

Funding

British Heart Foundation PG/15/12/31280Medical Research Council MR/K000888/1Medical Research Council MR/N000048/1
6 · The paper itself

Abstract

Mitochondrial homeostasis is maintained by removing dysfunctional, ubiquitinated mitochondria from the network via PRKN-dependent mitophagy. MYO6, a unique myosin that moves towards the minus ends of actin filaments, forms a complex with PRKN and is selectively recruited to damaged mitochondria by binding to ubiquitin. On the mitochondrial surface, this myosin motor initiates the assembly of F-actin cages, which serve as a quality control mechanism to isolate dysfunctional mitochondria thereby preventing their refusion with neighboring populations. MYO6 also plays a role in the later stages of the mitophagy pathway by tethering endosomes to actin filaments facilitating mitophagosome maturation and autophagosome-lysosome fusion.

Indexed as

AutophagyMitophagyActinsHeLa CellsHumansMitochondriaMyosin Heavy ChainsUbiquitin-Protein LigasesActinsMyosin Heavy Chainsmyosin VIUbiquitin-Protein LigasesActinmitochondrial quality controlmitophagyMYO6myosin VIParkinPRKN

Identifiers

PMID30058425
PMCPMC6135565
OpenAlexW2885220299

What Socratic 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 Socratic graph.