Evidence map›Paper›PMID 39145464›Full record

ReviewJournal of cell science2024

Conjugation of ATG8s to single membranes at a glance.

Carmen Figueras-Novoa, Lewis Timimi, Elena Marcassa, Rachel Ulferts, Rupert Beale

Abstract readReview
In one paragraph

Review in Journal of cell science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Full length TECPR1 displays 'cis' Dysferlin domain architecture.bioRxiv : the preprint server for biology · 2026
    Article
  11. Links Between Autophagy and Healthy Aging.Journal of molecular biology · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. ATG16L1 controls mammalian vacuolar proton ATPase.The Journal of cell biology · 2025
    Article
  18. A role for CASM in the repair of damaged Golgi architecture.bioRxiv : the preprint server for biology · 2025
    Article
  19. Article
  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

5 authors.

Carmen Figueras-NovoaCell Biology of Infection Laboratory, The Francis Crick Institute, London NW1 1AT, UK.ORCID 0009-0005-0115-3089
Lewis TimimiCell Biology of Infection Laboratory, The Francis Crick Institute, London NW1 1AT, UK.ORCID 0009-0004-7243-5983
Elena MarcassaCell Biology of Infection Laboratory, The Francis Crick Institute, London NW1 1AT, UK.ORCID 0000-0001-7176-644X
Rachel UlfertsCell Biology of Infection Laboratory, The Francis Crick Institute, London NW1 1AT, UK.ORCID 0000-0002-4810-9115
Rupert BealeCell Biology of Infection Laboratory, The Francis Crick Institute, London NW1 1AT, UK.ORCID 0000-0002-6705-8560

Funding

Cancer Research UKMedical Research CouncilThe Francis Crick InstituteWellcome Trust CC2087
6 · The paper itself

Abstract

Autophagy refers to a set of degradative mechanisms whereby cytoplasmic contents are targeted to the lysosome. This is best described for macroautophagy, where a double-membrane compartment (autophagosome) is generated to engulf cytoplasmic contents. Autophagosomes are decorated with ubiquitin-like ATG8 molecules (ATG8s), which are recruited through covalent lipidation, catalysed by the E3-ligase-like ATG16L1 complex. LC3 proteins are ATG8 family members that are often used as a marker for autophagosomes. In contrast to canonical macroautophagy, conjugation of ATG8s to single membranes (CASM) describes a group of non-canonical autophagy processes in which ATG8s are targeted to pre-existing single-membrane compartments. CASM occurs in response to disrupted intracellular pH gradients, when the V-ATPase proton pump recruits ATG16L1 in a process called V-ATPase-ATG16L1-induced LC3 lipidation (VAIL). Recent work has demonstrated a parallel, alternative axis for CASM induction, triggered when the membrane recruitment factor TECPR1 recognises sphingomyelin exposed on the cytosolic face of a membrane and forms an alternative E3-ligase-like complex. This sphingomyelin-TECPR1-induced LC3 lipidation (STIL) is independent of the V-ATPase and ATG16L1. In light of these discoveries, this Cell Science at a Glance article summarises these two mechanisms of CASM to highlight how they differ from canonical macroautophagy, and from each other.

Indexed as

AutophagyAutophagy-Related Protein 8 FamilyAnimalsAutophagosomesAutophagy-Related ProteinsCell MembraneHumansMicrotubule-Associated ProteinsAutophagy-Related Protein 8 FamilyAutophagy-Related ProteinsMicrotubule-Associated ProteinsATG8ylationAutophagyCASMSTILTECPR1VAILV-ATPase

Identifiers

PMID39145464
PMCPMC11361636

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.