Evidence map›Paper›PMID 28017329›Full record

ArticleCell2017

Prohibitin 2 Is an Inner Mitochondrial Membrane Mitophagy Receptor.

Yongjie Wei, Wei-Chung Chiang, Rhea Sumpter, Prashant Mishra, Beth Levine

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 522 papers.

0numbers the graph read from it
0cells of the map it votes in
522citing papers in PubMed
43.6field-weighted citation impact, top 1% 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

522 citing papers in PubMed, 812 citations in OpenAlex.

  1. Review
  2. Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026
    Review
  3. Mitophagy coordinates organelle crosstalk in health and diseases.Signal transduction and targeted therapy · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Autophagy Defects and Mitochondrial Retention in Erythroid Diseases.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

462 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Yongjie WeiCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA.
Wei-Chung ChiangCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA.
Rhea SumpterCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA.
Prashant MishraChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA.
Beth LevineCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75230, USA. Electronic address: beth.levine@utsouthwestern.edu.
Howard Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · USChildren's Medical Center · US

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Sandi Leigh Pruitt · 2010 to 2026
$53.7M
Genetic and Pathway Analysis CoreU19AI109725 · NIAID · WASHINGTON UNIVERSITY · PI VIRGIN, HERBERT W · 2014 to 2018
$32.7M
Beclin 1-Bcl-2 Interactions: Effects on AutophagyR01CA109618 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI LEVINE, BETH C · 2004 to 2014
$3.1M
Novel host factors in selective autophagy of virusesK08AI099150 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI SUMPTER, RHEA M · 2012 to 2014
$391k
NCI NIH HHS P30 CA142543NCI NIH HHS R01 CA109618NIAID NIH HHS K08 AI099150NIAID NIH HHS U19 AI109725
6 · The paper itself

Abstract

The removal of unwanted or damaged mitochondria by autophagy, a process called mitophagy, is essential for key events in development, cellular homeostasis, tumor suppression, and prevention of neurodegeneration and aging. However, the precise mechanisms of mitophagy remain uncertain. Here, we identify the inner mitochondrial membrane protein, prohibitin 2 (PHB2), as a crucial mitophagy receptor involved in targeting mitochondria for autophagic degradation. PHB2 binds the autophagosomal membrane-associated protein LC3 through an LC3-interaction region (LIR) domain upon mitochondrial depolarization and proteasome-dependent outer membrane rupture. PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the clearance of paternal mitochondria after embryonic fertilization in C. elegans. Our findings pinpoint a conserved mechanism of eukaryotic mitophagy and demonstrate a function of prohibitin 2 that may underlie its roles in physiology, aging, and disease.

Indexed as

AgingAnimalsAutophagosomesCaenorhabditis elegansCaenorhabditis elegans ProteinsEmbryo, NonmammalianMembrane ProteinsMitochondrial MembranesProhibitinsRepressor ProteinsCaenorhabditis elegans ProteinsLC3 protein, C elegansMembrane Proteinsprohibitin 2, C elegansProhibitinsRepressor Proteinsautophagymitophagyprohibitin 2

Identifiers

PMID28017329
PMCPMC5235968
OpenAlexW2562998505

What OpenQuestion holds

Textmetadata
LicenceTDM
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.