Evidence map›Paper›PMID 29634932›Full record

ArticleDevelopmental cell2018

The RAB11A-Positive Compartment Is a Primary Platform for Autophagosome Assembly Mediated by WIPI2 Recognition of PI3P-RAB11A.

Claudia Puri, Mariella Vicinanza, Avraham Ashkenazi, Matthew J Gratian, Qifeng Zhang, Carla F Bento, Maurizio Renna, Fiona M Menzies, David C Rubinsztein

Open access · hybridAbstract read
In one paragraph

Article in Developmental cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
15.7field-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

124 citing papers in PubMed, 206 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Where and how do mammalian cells shape autophagosomes?The Journal of biological chemistry · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Rab14 promotes Parkin-mediated mitophagy.Molecular biology of the cell · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. AFrontiers in genetics · 2025
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Claudia PuriDepartment of Medical Genetics, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Mariella VicinanzaDepartment of Medical Genetics, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Avraham AshkenaziDepartment of Medical Genetics, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Matthew J GratianCambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Qifeng ZhangBabraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK.
Carla F BentoDepartment of Medical Genetics, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Maurizio RennaDepartment of Medical Genetics, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
Fiona M MenziesDepartment of Medical Genetics, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK.
David C RubinszteinDepartment of Medical Genetics, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK; UK Dementia Research Institute, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, UK. Electronic address: dcr1000@cam.ac.uk.
Wellcome Trust · GBWellcome/MRC Cambridge Stem Cell Institute · GBBabraham Institute · GBUK Dementia Research Institute · GB

Funding

Medical Research Council UKDRI-2002Wellcome TrustWellcome Trust 095317/Z/11/Z
6 · The paper itself

Abstract

Autophagy is a critical pathway that degrades intracytoplasmic contents by engulfing them in double-membraned autophagosomes that are conjugated with LC3 family members. These membranes are specified by phosphatidylinositol 3-phosphate (PI3P), which recruits WIPI2, which, in turn, recruits ATG16L1 to specify the sites of LC3-conjugation. Conventionally, phosphatidylinositides act in concert with other proteins in targeting effectors to specific membranes. Here we describe that WIPI2 localizes to autophagic precursor membranes by binding RAB11A, a protein that specifies recycling endosomes, and that PI3P is formed on RAB11A-positive membranes upon starvation. Loss of RAB11A impairs the recruitment and assembly of the autophagic machinery. RAB11A-positive membranes are a primary direct platform for canonical autophagosome formation that enables autophagy of the transferrin receptor and damaged mitochondria. While this compartment may receive membrane inputs from other sources to enable autophagosome biogenesis, RAB11A-positive membranes appear to be a compartment from which autophagosomes evolve.

Indexed as

AutophagosomesAutophagyAutophagy-Related ProteinsCarrier ProteinsEndosomesHeLa CellsHumansMembrane ProteinsMicrotubule-Associated ProteinsPhosphate-Binding ProteinsPhosphatidylinositol PhosphatesProtein Transportrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsReceptors, TransferrinATG16L1 protein, humanAutophagy-Related ProteinsCarrier ProteinsMAP1LC3A protein, humanMembrane ProteinsMicrotubule-Associated ProteinsPhosphate-Binding Proteinsphosphatidylinositol 3-phosphatePhosphatidylinositol Phosphatesrab11 GTP-Binding Proteinsrab GTP-Binding ProteinsReceptors, TransferrinWIPI2 protein, humanautophagyautophagy platformmacroautophagymitophagyRAB11Arecycling endosometransferrin receptorWIPI2

Identifiers

PMID29634932
PMCPMC5896254
OpenAlexW2797185557

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.