Evidence map›Paper›PMID 16007153›Full record

ArticleOncogene2005

Mitochondrial localization of p53 during adenovirus infection and regulation of its activity by E1B-19K.

Elena Lomonosova, T Subramanian, G Chinnadurai

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. CD22Science China. Life sciences · 2026
    Article
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  4. Article
  5. Article
  6. Article
  7. Article
  8. Cancer immunotherapies: A hope for the uncurable?Frontiers in molecular medicine · 2023
    Review
  9. Article
  10. Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021
    Review
  11. Article
  12. Article
  13. Long story short: p53 mediates innate immunity.Biochimica et biophysica acta · 2016
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Improved potency and selectivity of an oncolytic E1ACR2 and E1B19K deleted adenoviral mutant in prostate and pancreatic cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010
    Article
  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

3 authors at 1 institution in 1 country.

Elena LomonosovaInstitute for Molecular Virology, Saint Louis University School of Medicine, 3681 Park Avenue, St Louis, MO 63110, USA.
T Subramanian
G Chinnadurai
Saint Louis University · US

Funding

PROMOTION OF CELL SURVIVAL BY ADENOVIRUS E1B 19K PROTEINR01CA033616 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1985 to 2015
$4.0M
NCI NIH HHS CA-33616NCI NIH HHS R01 CA033616
6 · The paper itself

Abstract

Recent results have revealed that the p53 tumor suppressor protein possesses a direct transcription-independent apoptotic activity. During apoptosis induced by genotoxic stress, a small fraction of p53 is targeted to mitochondria where it initiates apoptosis by causing mitochondrial dysfunction. In adenovirus-infected cells, the expression of E1A protein enhances the accumulation of p53 during early phases of infection and during late times after infection, it is targeted for degradation by the combined action of E1B-55K and E4-orf6 proteins. The functional significance of E1A-mediated accumulation of p53 during early phases of viral replication is not known. Our studies with isogenic epithelial cell lines that differ only on the status of p53 indicate that Ad infection induces apoptosis by p53-dependent and -independent pathways and both pathways are suppressed by E1B-19K. We show that during early phase of Ad infection, a fraction of p53 is targeted to the mitochondria. In virus infected cells, a large fraction of the viral antiapoptosis protein E1B-19K is also localized in mitochondria during early and late phases of infection. Coimmunoprecipitation analysis has revealed that p53 and E1B-19K form a complex in mitochondria. The interaction of 19K involves two noncontiguous regions located around amino-acid residues 14-15 and 123-124. On p53, the mutations within the DNA-binding domain reduce interaction with E1B-19K. Our studies also suggest that 19K may additionally complex with the multidomain mitochondrial proapoptotic protein BAK, thereby reducing the level of p53 interaction with BAK. We suggest that p53-induced apoptosis may be important for efficient cell lysis and viral spread and that E1B-19K may neutralize the apoptotic activity of p53 at multiple levels.

Indexed as

AdenoviridaeAdenovirus E1B ProteinsAmino Acid SequenceApoptosisbcl-2 Homologous Antagonist-Killer ProteinCell Line, TumorHumansImmunoprecipitationMitochondriaMolecular Sequence DataProtein BindingProtein TransportTumor Suppressor Protein p53Adenovirus E1B ProteinsBAK1 protein, humanbcl-2 Homologous Antagonist-Killer ProteinTumor Suppressor Protein p53

Identifiers

PMID16007153
OpenAlexW2052285697

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.