Evidence map›Paper›PMID 30309841›Full record

ArticleEMBO reports2018

NDP52 interacts with mitochondrial RNA poly(A) polymerase to promote mitophagy.

Norihiko Furuya, Soichiro Kakuta, Katsuhiko Sumiyoshi, Maya Ando, Risa Nonaka, Ayami Suzuki, Saiko Kazuno, Shinji Saiki, Nobutaka Hattori

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Mechanism and regulation of mitophagy in liver diseases: a review.Frontiers in cell and developmental biology · 2025
    Review
  6. Advances in the study of mitophagy in osteoarthritis.Journal of Zhejiang University. Science. B · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. SUMOylation targeting mitophagy in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. The Dawn of Mitophagy: What Do We Know by Now?Current neuropharmacology · 2021
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Norihiko FuruyaDivision for Development of Autophagy Modulating Drugs, Juntendo University Graduate School of Medicine, Tokyo, Japan nohuruya@juntendo.ac.jp nhattori@juntendo.ac.jp.ORCID 0000-0001-7695-4271
Soichiro KakutaLaboratory of Morphology and Image Analysis, Biomedical Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Katsuhiko SumiyoshiDepartment of Health and Nutrition Collage of Human Science, Tokiwa University, Ibaraki, Japan.
Maya AndoDepartment of Neurology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Risa NonakaResearch Institute for Diseases of Old Age, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Ayami SuzukiDepartment of Neurology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Saiko KazunoLaboratory of Proteomics and Biomolecular Science, Research Support Center, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Shinji SaikiDivision for Development of Autophagy Modulating Drugs, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University Graduate School of Medicine, Tokyo, Japan nohuruya@juntendo.ac.jp nhattori@juntendo.ac.jp.ORCID 0000-0002-2034-2556
Juntendo University · JPTokiwa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkin-mediated mitophagy is a quality control pathway that selectively removes damaged mitochondria via the autophagic machinery. Autophagic receptors, which interact with ubiquitin and Atg8 family proteins, contribute to the recognition of damaged mitochondria by autophagosomes. NDP52, an autophagy receptor, is required for autophagic engulfment of damaged mitochondria during mitochondrial uncoupler treatment. The N-terminal SKICH domain and C-terminal zinc finger motif of NDP52 are both required for its function in mitophagy. While the zinc finger motif contributes to poly-ubiquitin binding, the function of the SKICH domain remains unclear. Here, we show that NDP52 interacts with mitochondrial RNA poly(A) polymerase (MTPAP) via the SKICH domain. During mitophagy, NDP52 invades depolarized mitochondria and interacts with MTPAP dependent on the proteasome but independent of ubiquitin binding. Loss of MTPAP reduces NDP52-mediated mitophagy, and the NDP52-MTPAP complex attracts more LC3 than NDP52 alone. These results indicate that NDP52 and MTPAP form an autophagy receptor complex, which enhances autophagic elimination of damaged mitochondria.

Indexed as

MitophagyDNA-Directed RNA PolymerasesGene Knockdown TechniquesHeLa CellsHumansMitochondriaMitochondrial ProteinsMutationNuclear ProteinsPhagosomesProtein BindingProtein DomainsProtein Serine-Threonine KinasesUbiquitinUbiquitin-Protein LigasesValinomycinCALCOCO2 protein, humanDNA-Directed RNA PolymerasesMitochondrial ProteinsMTPAP protein, humanNuclear Proteinsparkin proteinProtein Serine-Threonine KinasesTBK1 protein, humanUbiquitinUbiquitin-Protein LigasesValinomycinmitophagyMTPAPNDP52ParkinSKICH domain

Identifiers

PMID30309841
PMCPMC6280801
OpenAlexW2896485223

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.