Evidence map›Paper›PMID 38001340›Full record

ArticleApoptosis : an international journal on programmed cell death2024

Cell-specific modulation of mitochondrial respiration and metabolism by the pro-apoptotic Bcl-2 family members Bax and Bak.

Dana Sovilj, Cristina Daniela Kelemen, Sarka Dvorakova, Renata Zobalova, Helena Raabova, Jan Kriska, Zuzana Hermanova, Tomas Knotek, Miroslava Anderova, Pavel Klener and 3 more

Abstract read
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In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Cells · 2025
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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

13 authors at 5 institutions in 3 countries.

Dana SoviljInstitute of Biotechnology, Czech Academy of Sciences, Vestec, Prague, Czech Republic.
Cristina Daniela KelemenInstitute of Biotechnology, Czech Academy of Sciences, Vestec, Prague, Czech Republic.
Sarka DvorakovaInstitute of Biotechnology, Czech Academy of Sciences, Vestec, Prague, Czech Republic.
Renata ZobalovaInstitute of Biotechnology, Czech Academy of Sciences, Vestec, Prague, Czech Republic.
Helena RaabovaInstitute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic.
Jan KriskaInstitute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
Zuzana HermanovaInstitute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
Tomas KnotekInstitute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
Miroslava AnderovaInstitute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
Pavel KlenerFirst Faculty of Medicine, Institute of Pathological Physiology, Charles University, Prague, Czech Republic.
Vlada FilimonenkoInstitute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic.
Jiri NeuzilInstitute of Biotechnology, Czech Academy of Sciences, Vestec, Prague, Czech Republic.
Ladislav AnderaInstitute of Biotechnology, Czech Academy of Sciences, Vestec, Prague, Czech Republic. Ladislav.andera@ibt.cas.cz.ORCID 0000-0003-3073-2280
Czech Academy of Sciences, Institute of Experimental Medicine · CZCzech Academy of Sciences · CZCzech Academy of Sciences, Institute of Biotechnology · CZCharles University · CZGriffith University · AU

Funding

Czech Academy of Sciences L200392251Czech Science Foundation GA19-08772SCzech Science Foundation GX21-04607XInstitute of Biotechnology 86652036Ministry of Education, Youth and Sports of the Czech Republic LM2023050Ministry of Health of the Czech Republic NU21-03-00386
6 · The paper itself

Abstract

Proteins from the Bcl-2 family play an essential role in the regulation of apoptosis. However, they also possess cell death-unrelated activities that are less well understood. This prompted us to study apoptosis-unrelated activities of the Bax and Bak, pro-apoptotic members of the Bcl-2 family. We prepared Bax/Bak-deficient human cancer cells of different origin and found that while respiration in the glioblastoma U87 Bax/Bak-deficient cells was greatly enhanced, respiration of Bax/Bak-deficient B lymphoma HBL-2 cells was slightly suppressed. Bax/Bak-deficient U87 cells also proliferated faster in culture, formed tumours more rapidly in mice, and showed modulation of metabolism with a considerably increased NAD

Indexed as

Apoptosisbcl-2 Homologous Antagonist-Killer ProteinAnimalsbcl-2-Associated X ProteinHumansMiceMitochondriaProto-Oncogene Proteins c-bcl-2Respirationbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinProto-Oncogene Proteins c-bcl-2BakBaxCell proliferationMetabolismMitochondrial respirationTEFM

Identifiers

PMID38001340
OpenAlexW4388966433

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.