Evidence map›Paper›PMID 30403914›Full record

ArticleAutophagy2019

The ATG5-binding and coiled coil domains of ATG16L1 maintain autophagy and tissue homeostasis in mice independently of the WD domain required for LC3-associated phagocytosis.

Shashank Rai, Maryam Arasteh, Matthew Jefferson, Timothy Pearson, Yingxue Wang, Weijiao Zhang, Bertalan Bicsak, Devina Divekar, Penny P Powell, Ronald Naumann and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. ATG16L1 controls mammalian vacuolar proton ATPase.The Journal of cell biology · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Autophagy and Bacterial infections.Autophagy reports · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. The WD Domain ofJID innovations : skin science from molecules to population health · 2024
    Article
  19. Article
  20. Article

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

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

15 authors at 4 institutions in 2 countries.

Shashank Raia Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Maryam Arasteha Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Matthew Jeffersona Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Timothy Pearsona Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Yingxue Wanga Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Weijiao Zhanga Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Bertalan Bicsaka Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Devina Divekara Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Penny P Powella Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
Ronald Naumannb Max-Planck-Institute of Molecular Cell Biology and Genetics , Dresden , Germany.
Naiara Berazac Quadram Institute Bioscience , Norwich , Norfolk , UK.
Simon R Cardingc Quadram Institute Bioscience , Norwich , Norfolk , UK.
Oliver Floreyd Signalling Programme , Babraham Institute , Cambridge , UK.
Ulrike Mayere School of Biological Sciences , University of East Anglia , Norwich , Norfolk, UK.ORCID 0000-0003-2328-0052
Thomas Wilemana Norwich Medical School , University of East Anglia , Norwich , Norfolk , UK.
University of East Anglia · GBQuadram Institute · GBBabraham Institute · GBMax Planck Institute of Molecular Cell Biology and Genetics · DE

Funding

Biotechnology and Biological Sciences Research Council BB/J004529/1Biotechnology and Biological Sciences Research Council BBS/E/F/000PR10353Biotechnology and Biological Sciences Research Council BBS/E/F/000PR10355Cancer Research UK 16337
6 · The paper itself

Abstract

Macroautophagy/autophagy delivers damaged proteins and organelles to lysosomes for degradation, and plays important roles in maintaining tissue homeostasis by reducing tissue damage. The translocation of LC3 to the limiting membrane of the phagophore, the precursor to the autophagosome, during autophagy provides a binding site for autophagy cargoes, and facilitates fusion with lysosomes. An autophagy-related pathway called LC3-associated phagocytosis (LAP) targets LC3 to phagosome and endosome membranes during uptake of bacterial and fungal pathogens, and targets LC3 to swollen endosomes containing particulate material or apoptotic cells. We have investigated the roles played by autophagy and LAP in vivo by exploiting the observation that the WD domain of ATG16L1 is required for LAP, but not autophagy. Mice lacking the linker and WD domains, activate autophagy, but are deficient in LAP. The LAP

Indexed as

AutophagyPhagocytosisAnimalsAutophagy-Related Protein 5Autophagy-Related ProteinsBrainCarrier ProteinsCytokinesFemaleFibroblastsHomeostasisKidneyLiverLongevityMacrophagesMaleAtg16l1 protein, mouseAtg5 protein, mouseAutophagy-Related Protein 5Autophagy-Related ProteinsCarrier ProteinsCytokinesMap1lc3b protein, mouseMicrotubule-Associated ProteinsATG16L1brainLC3-associated phagocytosissequestosome 1/p62 inclusionstissue homeostasisWD domainWIPI2

Identifiers

PMID30403914
PMCPMC6526875
OpenAlexW2896813617

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.