Evidence map›Paper›PMID 24886575›Full record

ArticleRetrovirology2014

HIV-1 protease-induced apoptosis.

Michaela Rumlová, Ivana Křížová, Alena Keprová, Romana Hadravová, Michal Doležal, Karolína Strohalmová, Iva Pichová, Miroslav Hájek, Tomáš Ruml

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Protease-mediated maturation of M-PMV reverse transcriptase into a functional heterodimer.Protein science : a publication of the Protein Society · 2026
    Article
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  4. Ferroptosis of T cell in inflammation and tumour immunity.Clinical and translational medicine · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Targeting HIV-1 reservoirs in T cell subsets.Frontiers in immunology · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 3 institutions in 1 country.

Michaela RumlováInstitute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, v,v,i,, IOCB & Gilead Research Center, Flemingovo nám, 2, 166 10 Prague, Czech Republic. rumlova@uochb.cas.cz.
Ivana Křížová
Alena Keprová
Romana Hadravová
Michal Doležal
Karolína Strohalmová
Iva Pichová
Miroslav Hájek
Tomáš Ruml
Czech Academy of Sciences, Institute of Organic Chemistry and Biochemistry · CZUniversity of Chemistry and Technology, Prague · CZCzech Academy of Sciences · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApoptosis is one of the presumptive causes of CD4+ T cell depletion during HIV infection and progression to AIDS. However, the precise role of HIV-1 in this process remains unexplained. HIV-1 protease (PR) has been suggested as a possible factor, but a direct link between HIV-1 PR enzymatic activity and apoptosis has not been established.

resultsHere, we show that expression of active HIV-1 PR induces death in HeLa and HEK-293 cells via the mitochondrial apoptotic pathway. This conclusion is based on in vivo observations of the direct localization of HIV-1 PR in mitochondria, a key player in triggering apoptosis. Moreover, we observed an HIV-1 PR concentration-dependent decrease in mitochondrial membrane potential and the role of HIV-1 PR in activation of caspase 9, PARP cleavage and DNA fragmentation. In addition, in vitro data demonstrated that HIV-1 PR mediates cleavage of mitochondrial proteins Tom22, VDAC and ANT, leading to release of AIF and Hsp60 proteins. By using yeast two-hybrid screening, we also identified a new HIV-1 PR interaction partner, breast carcinoma-associated protein 3 (BCA3). We found that BCA3 accelerates p53 transcriptional activity on the bax promoter, thus elevating the cellular level of pro-apoptotic Bax protein.

conclusionIn summary, our results describe the involvement of HIV-1 PR in apoptosis, which is caused either by a direct effect of HIV-1 PR on mitochondrial membrane integrity or by its interaction with cellular protein BCA3.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisbcl-2-Associated X ProteinCD4-Positive T-LymphocytesCell LineCell Line, TumorDNA FragmentationHEK293 CellsHeLa CellsHIV-1HIV InfectionsHIV ProteaseHumansMitochondriaMitochondrial ProteinsNuclear ProteinsAdaptor Proteins, Signal TransducingAKIP1 protein, humanBAX protein, humanbcl-2-Associated X ProteinHIV ProteaseMitochondrial ProteinsNuclear Proteinsp16 protease, Human immunodeficiency virus 1TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24886575
PMCPMC4229777
OpenAlexW2136500130

What OpenQuestion holds

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LicenceCC BY
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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.