Evidence map›Paper›PMID 23478020›Full record

ArticleCell reports2013

Suppression of host p53 is critical for Plasmodium liver-stage infection.

Alexis Kaushansky, Albert S Ye, Laura S Austin, Sebastian A Mikolajczak, Ashley M Vaughan, Nelly Camargo, Peter G Metzger, Alyse N Douglass, Gavin MacBeath, Stefan H I Kappe

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
  5. Oncology letters · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Mechanism of Immune Evasion in Mosquito-Borne Diseases.Pathogens (Basel, Switzerland) · 2023
    Review
  11. Ghrelin regulating liver activity and its potential effects on liver fibrosis andFrontiers in cellular and infection microbiology · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Recent Advances in Host-Directed Therapies for Tuberculosis and Malaria.Frontiers in cellular and infection microbiology · 2022
    Review
  20. Coding and Noncoding RNA Expression Profiles of Spleen CD4Contrast media & molecular imaging · 2022
    Article

9 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 1 country.

Alexis KaushanskyMalaria Program, Seattle Biomedical Research Institute, Seattle, WA 98109, USA.
Albert S Ye
Laura S Austin
Sebastian A Mikolajczak
Ashley M Vaughan
Nelly Camargo
Peter G Metzger
Alyse N Douglass
Gavin MacBeath
Stefan H I Kappe
Center for Infectious Disease Research · USCenter for Systems Biology · USHarvard University · USUniversity of Washington · US

Funding

Diseases of Public Health Importance Training GrantT32AI007509 · NIAID · UNIVERSITY OF WASHINGTON · PI LUND, JENNIFER M · 1997 to 2024
$6.3M
Investigating the Role of Cellular Signaling in Liver-Stage Malaria InfectionF32AI091129 · NIAID · SEATTLE BIOMEDICAL RESEARCH INSTITUTE · PI KAUSHANSKY, ALEXIS · 2010 to 2012
$156k
NIAID NIH HHS F32 AI091129NIAID NIH HHS T32 AI007509
6 · The paper itself

Abstract

Plasmodium parasites infect the liver and replicate inside hepatocytes before they invade erythrocytes and trigger clinical malaria. Analysis of host signaling pathways affected by liver-stage infection could provide critical insights into host-pathogen interactions and reveal targets for intervention. Using protein lysate microarrays, we found that Plasmodium yoelii rodent malaria parasites perturb hepatocyte regulatory pathways involved in cell survival, proliferation, and autophagy. Notably, the prodeath protein p53 was substantially decreased in infected hepatocytes, suggesting that it could be targeted by the parasite to foster survival. Indeed, mice that express increased levels of p53 showed reduced liver-stage parasite burden, whereas p53 knockout mice suffered increased liver-stage burden. Furthermore, boosting p53 levels with the use of the small molecule Nutlin-3 dramatically reduced liver-stage burden in vitro and in vivo. We conclude that perturbation of the hepatocyte p53 pathway critically impacts parasite survival. Thus, host pathways might constitute potential targets for host-based antimalarial prophylaxis.

Indexed as

AnimalsAutophagyCell ProliferationCell SurvivalHepatocytesHost-Parasite InteractionsImidazolesLife Cycle StagesLiverMiceMice, TransgenicMutationPiperazinesPlasmodium yoeliiProtein Array AnalysisTumor Suppressor Protein p53Imidazolesnutlin 3PiperazinesTumor Suppressor Protein p53

Identifiers

PMID23478020
PMCPMC3619000
OpenAlexW2133541091

What OpenQuestion holds

Textmetadata
LicenceTDM
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.