Evidence map›Paper›PMID 19343212›Full record

ArticlePLoS pathogens2009

MAPK ERK signaling regulates the TGF-beta1-dependent mosquito response to Plasmodium falciparum.

Win Surachetpong, Naresh Singh, Kong Wai Cheung, Shirley Luckhart

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

59 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Article
  7. Host complement C3 promotes malaria transmission by killing symbiotic bacteria in the mosquito midgut.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Histamine Ingestion byBiomolecules · 2021
    Article
  14. Vector Specificity of Arbovirus Transmission.Frontiers in microbiology · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Frontiers in cellular and infection microbiology · 2019
    Article
  20. Review
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

4 authors at 1 institution in 1 country.

Win SurachetpongDepartment of Medical Microbiology and Immunology, University of California Davis, Davis, CA, USA.
Naresh Singh
Kong Wai Cheung
Shirley Luckhart
University of California Davis Medical Center · US

Funding

Cross-talk among mosquito and mammalian immune factorsR01AI050663 · NIAID · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LUCKHART, SHIRLEY · 2004 to 2008
$1.6M
Cross-talk among mosquito and mammalian immune factorsR21AI050663 · NIAID · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI LUCKHART, SHIRLEY · 2002 to 2002
$292k
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR012088 · NCRR · UNIVERSITY OF CALIFORNIA DAVIS · PI CURRY, FITZ-ROY E · 1996 to 1996
–
NCRR NIH HHS C06 RR012088NCRR NIH HHS C06 RR-12088-01NIAID NIH HHS AI050663NIAID NIH HHS R01 AI050663NIAID NIH HHS R21 AI050663
6 · The paper itself

Abstract

Malaria is caused by infection with intraerythrocytic protozoa of the genus Plasmodium that are transmitted by Anopheles mosquitoes. Although a variety of anti-parasite effector genes have been identified in anopheline mosquitoes, little is known about the signaling pathways that regulate these responses during parasite development. Here we demonstrate that the MEK-ERK signaling pathway in Anopheles is controlled by ingested human TGF-beta1 and finely tunes mosquito innate immunity to parasite infection. Specifically, MEK-ERK signaling was dose-dependently induced in response to TGF-beta1 in immortalized cells in vitro and in the A. stephensi midgut epithelium in vivo. At the highest treatment dose of TGF-beta1, inhibition of ERK phosphorylation increased TGF-beta1-induced expression of the anti-parasite effector gene nitric oxide synthase (NOS), suggesting that increasing levels of ERK activation negatively feed back on induced NOS expression. At infection levels similar to those found in nature, inhibition of ERK activation reduced P. falciparum oocyst loads and infection prevalence in A. stephensi and enhanced TGF-beta1-mediated control of P. falciparum development. Taken together, our data demonstrate that malaria parasite development in the mosquito is regulated by a conserved MAPK signaling pathway that mediates the effects of an ingested cytokine.

Indexed as

MAP Kinase Signaling SystemAnalysis of VarianceAnimalsAnophelesCells, CulturedChi-Square DistributionExtracellular Signal-Regulated MAP KinasesGene Expression RegulationImmunity, InnateInsect ProteinsNitric Oxide Synthase Type IIPlasmodium falciparumSignal TransductionStatistics, NonparametricTransforming Growth Factor beta1Extracellular Signal-Regulated MAP KinasesInsect ProteinsNitric Oxide Synthase Type IITransforming Growth Factor beta1

Identifiers

PMID19343212
PMCPMC2658807
OpenAlexW1981203554

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.