Evidence map›Paper›PMID 19531803›Full record

ArticleScience signaling2009

Suppression of LPS-induced TNF-alpha production in macrophages by cAMP is mediated by PKA-AKAP95-p105.

Estelle A Wall, Joelle R Zavzavadjian, Mi Sook Chang, Baljinder Randhawa, Xiaocui Zhu, Robert C Hsueh, Jamie Liu, Adrienne Driver, Xiaoyan Robert Bao, Paul C Sternweis and 2 more

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

116 citing papers in PubMed, 183 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. The role of the incretin GIP in inflammation.Journal of endocrinological investigation · 2026
    Review
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  6. Article
  7. Article
  8. Review
  9. Review
  10. Inhibition of visceral adipose tissue-derived pathogenic signals by activation of adenosine AAmerican journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. MedComm · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article

56 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

12 authors at 2 institutions in 1 country.

Estelle A WallAlliance for Cellular Signaling, Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.
Joelle R Zavzavadjian
Mi Sook Chang
Baljinder Randhawa
Xiaocui Zhu
Robert C Hsueh
Jamie Liu
Adrienne Driver
Xiaoyan Robert Bao
Paul C Sternweis
Melvin I Simon
Iain D C Fraser
California Institute of Technology · USThe University of Texas Southwestern Medical Center · US

Funding

MICROFABRICATED DYNAMIC ARRY CYTOMETER FOR CELL SIGNALINU54GM062114 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI GRAY, MARTHA L · 2000 to 2007
$63.7M
RNAi Screening in Hematopoietic CellsZIAAI001106 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FRASER, IAIN · 2009 to 2025
$12.4M
Analysis of Innate Immune Signaling NetworksZIAAI001107 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FRASER, IAIN · 2009 to 2025
$11.9M
Intramural NIH HHS ZIA AI001106Intramural NIH HHS ZIA AI001107NIGMS NIH HHS U54 GM062114
6 · The paper itself

Abstract

The activation of macrophages through Toll-like receptor (TLR) pathways leads to the production of a broad array of cytokines and mediators that coordinate the immune response. The inflammatory potential of this response can be reduced by compounds, such as prostaglandin E(2), that induce the production of cyclic adenosine monophosphate (cAMP). Through experiments with cAMP analogs and multigene RNA interference (RNAi), we showed that key anti-inflammatory effects of cAMP were mediated specifically by cAMP-dependent protein kinase (PKA). Selective inhibitors of PKA anchoring, time-lapse microscopy, and RNAi screening suggested that differential mechanisms of PKA action existed. We showed a specific role for A kinase-anchoring protein 95 in suppressing the expression of the gene encoding tumor necrosis factor-alpha, which involved phosphorylation of p105 (also known as Nfkb1) by PKA at a site adjacent to the region targeted by inhibitor of nuclear factor kappaB kinases. These data suggest that crosstalk between the TLR4 and cAMP pathways in macrophages can be coordinated through PKA-dependent scaffolds that localize specific pools of the kinase to distinct substrates.

Indexed as

A Kinase Anchor ProteinsAnimalsCell LineCyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneGene Expression RegulationInflammationLipopolysaccharidesMacrophagesMiceNF-kappa B p50 SubunitPhosphorylationRNA InterferenceSecond Messenger SystemsToll-Like Receptor 4A Kinase Anchor ProteinsCyclic AMPCyclic AMP-Dependent Protein KinasesDinoprostoneLipopolysaccharidesNF-kappa B p50 SubunitNfkb1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID19531803
PMCPMC2770900
OpenAlexW2153744286

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.