Evidence map›Paper›PMID 10417174›Full record

ArticleInfection and immunity1999

Activation of phosphotyrosine phosphatase activity attenuates mitogen-activated protein kinase signaling and inhibits c-FOS and nitric oxide synthase expression in macrophages infected with Leishmania donovani.

D Nandan, R Lo, N E Reiner

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 143 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
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  7. Article
  8. Chromatin-Remodeling Factor BRG1 Is a Negative Modulator ofFrontiers in cellular and infection microbiology · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. Frontiers in microbiology · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. The genetics of Leishmania virulence.Medical microbiology and immunology · 2015
    Review
  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 2 countries.

D NandanDepartment of Medicine (Division of Infectious Diseases), Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada V5Z 3J5.
R Lo
N E Reiner
Vancouver Hospital and Health Sciences Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular protozoan parasites of the genus Leishmania antagonize host defense mechanisms by interfering with cell signaling in macrophages. In this report, the impact of Leishmania donovani on mitogen-activated protein (MAP) kinases and nitric oxide synthase (NOS) expression in the macrophage cell line RAW 264 was investigated. Overnight infection of cells with leishmania led to a significant decrease in phorbol-12-myristate-13-acetate (PMA)-stimulated MAP kinase activity and inhibited PMA-induced phosphorylation of the MAP kinase substrate and transcription factor Elk-1. Simultaneously, leishmania infection markedly attenuated the induction of c-FOS and inducible nitric oxide synthase (iNOS) expression in response to PMA and gamma interferon (IFN-gamma), respectively. These effects correlated with decreased phosphorylation of p44 and p42 MAP kinases on tyrosine residues. Consistent with the latter finding, lysates prepared from leishmania-infected cells contained an activity that dephosphorylated MAP kinase in vitro, suggesting the possibility of a phosphatase acting in vivo. Attenuation of both MAP kinase activity and c-FOS and iNOS expression was reversed by treatment of macrophages with sodium orthovanadate prior to infection. It was also found that the specific activity of the Src homology 2 domain containing tyrosine phosphatase (SHP-1) toward MAP kinase was markedly increased in leishmania-infected cells. These findings indicate that infection with L. donovani attenuates MAP kinase signaling and c-FOS and iNOS expression in macrophages by activating cellular phosphotyrosine phosphatases. This may represent a novel mechanism of macrophage deactivation during intracellular infection.

Indexed as

DNA-Binding ProteinsTranscription FactorsAnimalsCalcium-Calmodulin-Dependent Protein KinasesCell LineEnzyme Activationets-Domain Protein Elk-1Intracellular Signaling Peptides and ProteinsLeishmania donovaniMacrophagesMiceNitric Oxide SynthaseNitric Oxide Synthase Type IIPhosphorylationProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Calcium-Calmodulin-Dependent Protein KinasesDNA-Binding ProteinsElk1 protein, mouseets-Domain Protein Elk-1Intracellular Signaling Peptides and ProteinsNitric Oxide SynthaseNitric Oxide Synthase Type IINos2 protein, mouseProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesProto-Oncogene ProteinsProto-Oncogene Proteins c-fosPtpn11 protein, mousePtpn6 protein, mouseTetradecanoylphorbol AcetateTranscription FactorsTyrosine

Identifiers

PMID10417174
PMCPMC96702
OpenAlexW2098875897

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.