Evidence map›Paper›PMID 42056306›Full record

ArticleNature structural & molecular biology2026

MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth.

Hector Flores-Romero, Aida Pena-Blanco, Jonas Aufdermauer, Shashank Dadsena, Philip Neubert, Lisa Hohorst, Eileen Cors, Cristiana Zollo, Alvaro Larrañaga-SanMiguel, Jone Zaldunbide and 5 more

Abstract read
In one paragraph

Article in Nature structural & molecular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth.Nature structural & molecular biology · 2026
    Article
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

15 authors.

Hector Flores-Romero *Institute for Genetics and CECAD, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0003-0996-5717
Aida Pena-Blanco *Interfaculty Institute of Biochemistry, University of Tübingen, Tübingen, Germany.
Jonas Aufdermauer *Institute for Genetics and CECAD, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0009-0003-7028-1135
Shashank DadsenaInstitute for Genetics and CECAD, University of Cologne, Cologne, Germany.
Philip NeubertInstitute of Medical Microbiology and Hygiene, Medical Center, University of Freiburg, Faculty of Medicine, Freiburg, Germany.ORCID http://orcid.org/0009-0006-8023-4561
Lisa HohorstInstitute for Genetics and CECAD, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-2444-076X
Eileen CorsMax Planck Institute for Biology of Ageing, Cologne, Germany.
Cristiana ZolloInstitute for Genetics and CECAD, University of Cologne, Cologne, Germany.
Alvaro Larrañaga-SanMiguelAchucarro Basque Center for Neuroscience, Leioa, Spain.
Jone ZaldunbideAchucarro Basque Center for Neuroscience, Leioa, Spain.
Maria NenchovaInstitute for Genetics and CECAD, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0009-0008-2522-9641
Yasmin Carvalho-SchaeferInstitute for Genetics and CECAD, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0009-0007-5978-8858
Thomas LangerMax Planck Institute for Biology of Ageing, Cologne, Germany.
Georg HäckerInstitute of Medical Microbiology and Hygiene, Medical Center, University of Freiburg, Faculty of Medicine, Freiburg, Germany.
Ana J Garcia-SaezInstitute for Genetics and CECAD, University of Cologne, Cologne, Germany. ana.garcia@biophys.mpg.de.ORCID http://orcid.org/0000-0002-3894-5945

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During apoptosis, the BCL-2 family members BAX and BAK oligomerize and form a pore to mediate the decisive step of mitochondrial outer membrane permeabilization. However, the contribution of additional cellular components to apoptotic pore dynamics remains poorly understood. Here we map the protein environment of the apoptotic pore using in situ proximity labeling and identify the mitochondrial carrier homolog protein MTCH2 localizing nearby BAX and BAK assemblies specifically under apoptotic conditions. We show that cells lacking MTCH2 exhibit delayed BAX and BAK oligomerization at the single-particle level, which can be rescued by addition of lysophosphatidic acid. Accordingly, MTCH2 depletion decreases not only apoptosis sensitivity but also sublethal mitochondrial permeabilization during bacterial infection, mitochondrial DNA release into the cytosol and cGAS-STING activation under impaired caspases. Our findings uncover a key role of MTCH2 in promoting BAX and BAK high-order assembly with functional consequences for apoptotic pore growth and downstream responses.

Indexed as

Apoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinMitochondrial Membrane Transport ProteinsAnimalscGAS-STING Signaling PathwayHumansLysophospholipidsMiceMitochondriaMitochondrial MembranesProtein Multimerizationbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer Proteinlysophosphatidic acidLysophospholipidsMitochondrial Membrane Transport Proteins

Identifiers

PMID42056306
PMCPMC13186707

What OpenQuestion holds

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Registered trials

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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.