Evidence map›Paper›PMID 23852373›Full record

ArticleCell death and differentiation2014

Molecular mechanisms of ATP secretion during immunogenic cell death.

I Martins, Y Wang, M Michaud, Y Ma, A Q Sukkurwala, S Shen, O Kepp, D Métivier, L Galluzzi, J-L Perfettini and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 312 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
312citing papers in PubMed, 2 pooled it
18.7field-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

312 citing papers in PubMed, 2 syntheses or guidelines pooled it, 522 citations in OpenAlex.

  1. Pooled it
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  12. Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026
    Review
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  14. HIF-Regulated Pannexin-1 Channel Drives Luminal ATP Accumulation in Kidney Cysts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  20. Therapeutic Effects ofInternational journal of molecular sciences · 2026
    Article

252 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

12 authors at 6 institutions in 1 country.

I Martins1] INSERM, U848, F-94805 Villejuif, France [2] Institut Gustave Roussy, F-94805 Villejuif, France [3] Université Paris Sud/Paris XI, F-94270 Le Kremlin Bicêtre, France.
Y Wang
M Michaud
Y Ma
A Q Sukkurwala
S Shen
O Kepp
D Métivier
L Galluzzi
J-L Perfettini
L Zitvogel
G Kroemer
Université Paris-Saclay · FRInserm · FRInstitut Gustave Roussy · FRUniversité Paris-Sud · FRSorbonne Paris Cité · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immunogenic demise of cancer cells can be induced by various chemotherapeutics, such as anthracyclines and oxaliplatin, and provokes an immune response against tumor-associated antigens. Thus, immunogenic cell death (ICD)-inducing antineoplastic agents stimulate a tumor-specific immune response that determines the long-term success of therapy. The release of ATP from dying cells constitutes one of the three major hallmarks of ICD and occurs independently of the two others, namely, the pre-apoptotic exposure of calreticulin on the cell surface and the postmortem release of high-mobility group box 1 (HMBG1) into the extracellular space. Pre-mortem autophagy is known to be required for the ICD-associated secretion of ATP, implying that autophagy-deficient cancer cells fail to elicit therapy-relevant immune responses in vivo. However, the precise molecular mechanisms whereby ATP is actively secreted in the course of ICD remain elusive. Using a combination of pharmacological screens, silencing experiments and techniques to monitor the subcellular localization of ATP, we show here that, in response to ICD inducers, ATP redistributes from lysosomes to autolysosomes and is secreted by a mechanism that requires the lysosomal protein LAMP1, which translocates to the plasma membrane in a strictly caspase-dependent manner. The secretion of ATP additionally involves the caspase-dependent activation of Rho-associated, coiled-coil containing protein kinase 1 (ROCK1)-mediated, myosin II-dependent cellular blebbing, as well as the opening of pannexin 1 (PANX1) channels, which is also triggered by caspases. Of note, although autophagy and LAMP1 fail to influence PANX1 channel opening, PANX1 is required for the ICD-associated translocation of LAMP1 to the plasma membrane. Altogether, these findings suggest that caspase- and PANX1-dependent lysosomal exocytosis has an essential role in ATP release as triggered by immunogenic chemotherapy.

Indexed as

Adenosine TriphosphateAnimalsAntineoplastic AgentsAutophagy-Related Protein 5Cell DeathCell Line, TumorCell MembraneConnexinsDNA-Binding ProteinsHMGB1 ProteinHumansLysosomal-Associated Membrane Protein 1LysosomesMiceMicrotubule-Associated ProteinsMyosin Type IIAdenosine TriphosphateAntineoplastic AgentsATG5 protein, humanAutophagy-Related Protein 5ConnexinsCSDE1 protein, humanDNA-Binding ProteinsHMGB1 ProteinLysosomal-Associated Membrane Protein 1Microtubule-Associated ProteinsMyosin Type IINerve Tissue ProteinsPANX1 protein, humanrho-Associated KinasesRNA-Binding ProteinsRNA, Small InterferingROCK1 protein, human

Identifiers

PMID23852373
PMCPMC3857631
OpenAlexW1991505853

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.