Evidence map›Paper›PMID 35120587›Full record

ArticleMolecular cell2022

The interplay between BAX and BAK tunes apoptotic pore growth to control mitochondrial-DNA-mediated inflammation.

Katia Cosentino, Vanessa Hertlein, Andreas Jenner, Timo Dellmann, Milos Gojkovic, Aida Peña-Blanco, Shashank Dadsena, Noel Wajngarten, John S H Danial, Jervis Vermal Thevathasan and 3 more

Abstract read
In one paragraph

Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing 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

139 citing papers in PubMed.

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  8. Translational cancer research · 2026
    Article
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  15. Review
  16. Article
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  18. MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth.Nature structural & molecular biology · 2026
    Article
  19. Review
  20. Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Katia CosentinoInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany; Department of Biology/Chemistry and Center for Cellular Nanoanalytics (CellNanOs), University of Osnabrück, 49076 Osnabrück, Germany.
Vanessa HertleinInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany.
Andreas JennerInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany; Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Timo DellmannInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Milos GojkovicInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Aida Peña-BlancoInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany.
Shashank DadsenaInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Noel WajngartenInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany.
John S H DanialInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany.
Jervis Vermal ThevathasanCell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany.
Markus MundCell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany.
Jonas RiesCell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany.
Ana J Garcia-SaezInterfaculty Institute of Biochemistry, University of Tübingen, 72076 Tübingen, Germany; Institute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany. Electronic address: ana.garcia@uni-koeln.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BAX and BAK are key apoptosis regulators that mediate the decisive step of mitochondrial outer membrane permeabilization. However, the mechanism by which they assemble the apoptotic pore remains obscure. Here, we report that BAX and BAK present distinct oligomerization properties, with BAK organizing into smaller structures with faster kinetics than BAX. BAK recruits and accelerates BAX assembly into oligomers that continue to grow during apoptosis. As a result, BAX and BAK regulate each other as they co-assemble into the same apoptotic pores, which we visualize. The relative availability of BAX and BAK molecules thereby determines the growth rate of the apoptotic pore and the relative kinetics by which mitochondrial contents, most notably mtDNA, are released. This feature of BAX and BAK results in distinct activation kinetics of the cGAS/STING pathway with implications for mtDNA-mediated paracrine inflammatory signaling.

Indexed as

DNA, MitochondrialMitochondriaAnimalsApoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCell Line, TumorHumansInflammationProtein MultimerizationBAK1 protein, humanBAX protein, humanbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinDNA, MitochondrialAFMBAKBAXBCL-2inflammatory cell deathmembrane poremitochondriapore-forming proteinsingle-molecule imagingsuper-resolution microscopy

Identifiers

PMID35120587
PMCPMC8901441

What OpenQuestion holds

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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.