Evidence map›Paper›PMID 33082312›Full record

ArticleNature communications2020

Wipi3 is essential for alternative autophagy and its loss causes neurodegeneration.

Hirofumi Yamaguchi, Shinya Honda, Satoru Torii, Kimiko Shimizu, Kaoru Katoh, Koichi Miyake, Noriko Miyake, Nobuhiro Fujikake, Hajime Tajima Sakurai, Satoko Arakawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Functional Homology of WIPI4 and Atg18 EnablesInternational journal of molecular sciences · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. The Role of the Beclin1 Complex in Rab9-Dependent Alternative Autophagy.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. The p53 target DRAM1 modulates calcium homeostasis and ER stress by promoting contact between lysosomes and the ER through STIM1.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Physiological functions of ULK1/2.Journal of molecular biology · 2024
    Review
  18. Article
  19. Review
  20. Mitophagy for cardioprotection.Basic research in cardiology · 2023
    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

11 authors at 4 institutions in 1 country.

Hirofumi YamaguchiDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Shinya HondaDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.ORCID 0000-0003-3443-044X
Satoru ToriiDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.ORCID 0000-0003-4841-7131
Kimiko ShimizuDepartment of Biological Sciences, School of Science, The University of Tokyo, Tokyo, 113-0033, Japan.ORCID 0000-0003-4943-2552
Kaoru KatohBiomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), 1-1-1 Higashi, Tsukuba, Ibaraki, 305-8566, Japan.
Koichi MiyakeDepartment of Biochemistry and Molecular Biology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan.
Noriko MiyakeDepartment of Biochemistry and Molecular Biology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan.
Nobuhiro FujikakeDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Hajime Tajima SakuraiDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Satoko ArakawaDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. arako.pcb@mri.tmd.ac.jp.
Shigeomi ShimizuDepartment of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. shimizu.pcb@mri.tmd.ac.jp.ORCID 0000-0002-8437-0791
Tokyo Medical and Dental University · JPNippon Medical School · JPNational Institute of Advanced Industrial Science and Technology · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alternative autophagy is an Atg5/Atg7-independent type of autophagy that contributes to various physiological events. We here identify Wipi3 as a molecule essential for alternative autophagy, but which plays minor roles in canonical autophagy. Wipi3 binds to Golgi membranes and is required for the generation of isolation membranes. We establish neuron-specific Wipi3-deficient mice, which show behavioral defects, mainly as a result of cerebellar neuronal loss. The accumulation of iron and ceruloplasmin is also found in the neuronal cells. These abnormalities are suppressed by the expression of Dram1, which is another crucial molecule for alternative autophagy. Although Atg7-deficient mice show similar phenotypes to Wipi3-deficient mice, electron microscopic analysis shows that they have completely different subcellular morphologies, including the morphology of organelles. Furthermore, most Atg7/Wipi3 double-deficient mice are embryonic lethal, indicating that Wipi3 functions to maintain neuronal cells via mechanisms different from those of canonical autophagy.

Indexed as

AutophagyAnimalsAutophagy-Related Protein 5Autophagy-Related Protein 7FemaleGolgi ApparatusHumansMaleMembrane ProteinsMiceMice, Inbred C57BLNeurodegenerative DiseasesAutophagy-Related Protein 5Autophagy-Related Protein 7DRAM-1 protein, mouseMembrane Proteins

Identifiers

PMID33082312
PMCPMC7576787
OpenAlexW3094582012

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.