Evidence map›Paper›PMID 25484071›Full record

ArticleAutophagy2015

V-ATPase and osmotic imbalances activate endolysosomal LC3 lipidation.

Oliver Florey, Noor Gammoh, Sung Eun Kim, Xuejun Jiang, Michael Overholtzer

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 5% 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

148 citing papers in PubMed, 2 syntheses or guidelines pooled it, 227 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. A role for CASM in the repair of damaged Golgi architecture.bioRxiv : the preprint server for biology · 2025
    Article
  11. Review
  12. LYVAC/PDZD8 is a lysosomal vacuolator.Science (New York, N.Y.) · 2025
    Article
  13. Review
  14. Cell-Type-Specific Autophagy in Human Leukocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  15. Article
  16. Lysosomal Repair in Health and Disease.Journal of cellular physiology · 2025
    Review
  17. Article
  18. Review
  19. Review
  20. Article

88 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

5 authors at 2 institutions in 2 countries.

Oliver Floreya Cell Biology Program; Memorial Sloan-Kettering Cancer Center ; New York , NY USA.
Noor Gammoh
Sung Eun Kim
Xuejun Jiang
Michael Overholtzer
Memorial Sloan Kettering Cancer Center · USCornell University · US

Funding

Mechanisms and Function of Autophagy in CancerR01CA166413 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JIANG, XUEJUN · 2013 to 2023
$3.9M
The role of entosis in human cancersR01CA154649 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI OVERHOLTZER, MICHAEL H. · 2011 to 2020
$3.9M
Molecular Basis of Autophagy and Its Role in CancerF32CA162691 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI GAMMOH, NOOR · 2011 to 2013
$96k
Cancer Research UK 16337Cancer Research UK C47718/A16337NCI NIH HHS 1F32CA162691NCI NIH HHS R01 CA154649NCI NIH HHS R01CA154649NCI NIH HHS R01 CA166413NCI NIH HHS R01CA166413
6 · The paper itself

Abstract

Recently a noncanonical activity of autophagy proteins has been discovered that targets lipidation of microtubule-associated protein 1 light chain 3 (LC3) onto macroendocytic vacuoles, including macropinosomes, phagosomes, and entotic vacuoles. While this pathway is distinct from canonical autophagy, the mechanism of how these nonautophagic membranes are targeted for LC3 lipidation remains unclear. Here we present evidence that this pathway requires activity of the vacuolar-type H(+)-ATPase (V-ATPase) and is induced by osmotic imbalances within endolysosomal compartments. LC3 lipidation by this mechanism is induced by treatment of cells with the lysosomotropic agent chloroquine, and through exposure to the Heliobacter pylori pore-forming toxin VacA. These data add novel mechanistic insights into the regulation of noncanonical LC3 lipidation and its associated processes, including LC3-associated phagocytosis (LAP), and demonstrate that the widely and therapeutically used drug chloroquine, which is conventionally used to inhibit autophagy flux, is an inducer of LC3 lipidation.

Indexed as

OsmosisAnimalsAutophagyBacterial ProteinsCell LineChloroquineEndosomesEntosisHumansLipidsLysosomesMiceMicrotubule-Associated ProteinsMonensinPhagocytosisPhosphatidylinositol PhosphatesBacterial ProteinsChloroquineLipidsMAP1LC3A protein, humanMicrotubule-Associated ProteinsMonensinphosphatidylinositol 3-phosphatePhosphatidylinositol PhosphatesVacA protein, Helicobacter pyloriVacuolar Proton-Translocating ATPasesWaterATG, autophagy-relatedautophagyBaf, bafilomycin A1CALCOCO2/NDP52, calcium binding and coiled-coil domain 2catalytic subunit type 3chloroquineConA, concanamycin ACQ, chloroquineentosisFYCO1, FYVE and coiled-coil domain containing 1GFP, green fluorescent proteinHelicobacter pyloriLAMP1, lysosomal-associated membrane protein 1LAPLAP, LC3-associated phagocytosisLC3lysosomeMAP1LC3/LC3, microtubule-associated protein 1 light chain 3MTOR, mechanistic target of rapamycinphagocytosisPIK3C3/VPS34, phosphatidylinositol 3-kinasePtdIns3K, phosphatidylinositol 3-kinasePtdIns3P, phosphatidylinositol 3-phosphateRB1CC1/FIP200, RB1-inducible coiled-coil 1SQSTM1/p62, sequestosome 1TEM, transmission electron microscopyTLR, toll-like receptorULK1/2, unc-51 like autophagy activating kinase 1/2VacA, vacuolating toxin AV-ATPaseV-ATPase, vacuolar-type H+-ATPase

Identifiers

PMID25484071
PMCPMC4502810
OpenAlexW2154311364

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.