Evidence map›Paper›PMID 16103161›Full record

ArticleJournal of virology2005

Down-regulation of p53 by double-stranded RNA modulates the antiviral response.

Joao T Marques, Dominique Rebouillat, Chilakamarti V Ramana, Junko Murakami, Jason E Hill, Andrei Gudkov, Robert H Silverman, George R Stark, Bryan R G Williams

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. 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
3.7field-weighted citation impact, top 7% 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, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020
    Review
  5. Article
  6. Article
  7. PKR: A Kinase to Remember.Frontiers in molecular neuroscience · 2018
    Review
  8. Article
  9. Review
  10. PI3K/Akt/p53 pathway inhibits reovirus infection.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. PKR, a p53 target gene, plays a crucial role in the tumor-suppressor function of p53.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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 2 countries.

Joao T MarquesDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, OH 44195, USA.
Dominique Rebouillat
Chilakamarti V Ramana
Junko Murakami
Jason E Hill
Andrei Gudkov
Robert H Silverman
George R Stark
Bryan R G Williams
Cleveland Clinic · USMazda Motor Corporation (Japan) · JPYale University · US

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA, STARK, GEORGE ROBERT · 1994 to 2020
$35.6M
REGULATION OF INTERFERON-INDUCED DSRNA-ACTIVATED KINASER01AI034039 · NIAID · MONASH UNIVERSITY · PI WILLIAMS, BRYAN R. G. · 1993 to 2008
$2.5M
NCI NIH HHS P01 CA062220NCI NIH HHS P01 CA62220NIAID NIH HHS R01 AI034039NIAID NIH HHS R01 AI34039
6 · The paper itself

Abstract

p53 has been well characterized as a tumor suppressor gene, but its role in antiviral defense remains unclear. A recent report has demonstrated that p53 can be induced by interferons and is activated after vesicular stomatitis virus (VSV) infection. We observed that different nononcogenic viruses, including encephalomyocarditis virus (EMCV) and human parainfluenza virus type 3 (HPIV3), induced down-regulation of p53 in infected cells. Double-stranded RNA (dsRNA) and a mutant vaccinia virus lacking the dsRNA binding protein E3L can also induce this effect, indicating that dsRNA formed during viral infection is likely the trigger for down-regulation of p53. The mechanism of down-regulation of p53 by dsRNA relies on translation inhibition mediated by the PKR and RNase L pathways. In the absence of p53, the replication of both EMCV and HPIV3 was retarded, whereas, conversely, VSV replication was enhanced. Cell cycle analysis indicated that wild-type (WT) but not p53 knockout (KO) fibroblasts undergo an early-G(1) arrest following dsRNA treatment. Moreover, in WT cells the onset of dsRNA-induced apoptosis begins after p53 levels are down-regulated, whereas p53 KO cells, which lack the early-G(1) arrest, rapidly undergo apoptosis. Hence, our data suggest that the down-regulation of p53 facilitates apoptosis, thereby limiting viral replication.

Indexed as

AnimalsCells, CulturedDown-RegulationeIF-2 KinaseEncephalomyocarditis virusEndoribonucleasesParainfluenza Virus 3, HumanTumor Suppressor Protein p53Vesicular stomatitis Indiana virusVirus Replication2-5A-dependent ribonucleaseeIF-2 KinaseEndoribonucleasesTumor Suppressor Protein p53

Identifiers

PMID16103161
PMCPMC1193603
OpenAlexW2092841570

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.