Evidence map›Paper›PMID 33052098›Full record

ArticleeLife2020

Single-cell dynamics of pannexin-1-facilitated programmed ATP loss during apoptosis.

Hiromi Imamura, Shuichiro Sakamoto, Tomoki Yoshida, Yusuke Matsui, Silvia Penuela, Dale W Laird, Shin Mizukami, Kazuya Kikuchi, Akira Kakizuka

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  4. Anti-Aging Potential of Avocado Oil via Its Antioxidant Effects.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
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  12. Review
  13. Optimal inference of molecular interaction dynamics in FRET microscopy.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Article
  15. Article
  16. Pannexin1 channels in the liver: an open enemy.Frontiers in cell and developmental biology · 2023
    Review
  17. Article
  18. Article
  19. Review
  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

9 authors at 4 institutions in 2 countries.

Hiromi Imamura *Graduate School of Biostudies, Kyoto University, Kyoto, Japan.ORCID 0000-0002-1896-0443
Shuichiro Sakamoto *Graduate School of Biostudies, Kyoto University, Kyoto, Japan.
Tomoki YoshidaGraduate School of Biostudies, Kyoto University, Kyoto, Japan.
Yusuke MatsuiGraduate School of Engineering, Osaka University, Suita, Japan.
Silvia PenuelaDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada.ORCID 0000-0003-4829-5517
Dale W LairdDepartment of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada.
Shin MizukamiInstitute of Multidisciplinary Research for Advanced Materials, Tohoku University, Sendai, Japan.
Kazuya KikuchiGraduate School of Engineering, Osaka University, Suita, Japan.
Akira KakizukaGraduate School of Biostudies, Kyoto University, Kyoto, Japan.ORCID 0000-0003-3513-0334
Kyoto University · JPThe University of Osaka · JPWestern University · CATohoku University · JP

Funding

Japan Society for the Promotion of Science 16K14709Japan Society for the Promotion of Science 22687011Japan Society for the Promotion of Science 24657101
6 · The paper itself

Abstract

ATP is essential for all living cells. However, how dead cells lose ATP has not been well investigated. In this study, we developed new FRET biosensors for dual imaging of intracellular ATP level and caspase-3 activity in single apoptotic cultured human cells. We show that the cytosolic ATP level starts to decrease immediately after the activation of caspase-3, and this process is completed typically within 2 hr. The ATP decrease was facilitated by caspase-dependent cleavage of the plasma membrane channel pannexin-1, indicating that the intracellular decrease of the apoptotic cell is a 'programmed' process. Apoptotic cells deficient of pannexin-1 sustained the ability to produce ATP through glycolysis and to consume ATP, and did not stop wasting glucose much longer period than normal apoptotic cells. Thus, the pannexin-1 plays a role in arresting the metabolic activity of dead apoptotic cells, most likely through facilitating the loss of intracellular ATP.

Indexed as

Adenosine TriphosphateApoptosisCaspase 3ConnexinsHeLa CellsHumansNerve Tissue ProteinsSingle-Cell AnalysisAdenosine TriphosphateCASP3 protein, humanCaspase 3ConnexinsNerve Tissue ProteinsPANX1 protein, humanbiosensorcell biologycell deathenergy metabolismFREThumanimaging

Identifiers

PMID33052098
PMCPMC7556867
OpenAlexW3092266223

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.