Evidence map›Paper›PMID 11082122›Full record

ArticleBritish journal of pharmacology2000

p38 MAP kinase and MKK-1 co-operate in the generation of GM-CSF from LPS-stimulated human monocytes by an NF-kappa B-independent mechanism.

K K Meja, P M Seldon, Y Nasuhara, K Ito, P J Barnes, M A Lindsay, M A Giembycz

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Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-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

24 citing papers in PubMed, 71 citations in OpenAlex.

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  16. Identifying targets for COPD treatment through gene expression analyses.International journal of chronic obstructive pulmonary disease · 2008
    Review
  17. Article
  18. Article
  19. Future therapeutic treatment of COPD: struggle between oxidants and cytokines.International journal of chronic obstructive pulmonary disease · 2007
    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

7 authors at 3 institutions in 3 countries.

K K MejaThoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse Street, SW3 6LY.
P M Seldon
Y Nasuhara
K Ito
P J Barnes
M A Lindsay
M A Giembycz
Lung Institute · USHokkaido University · JPUniversity of Oxford · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. The extent to which the p38 mitogen-activated protein (MAP) kinase and MAP kinase kinase (MKK)-1-signalling pathways regulate the expression of granulocyte/macrophage colony-stimulating factor (GM-CSF) from LPS-stimulated human monocytes has been investigated and compared to the well studied cytokine tumour necrosis factor-alpha (TNF alpha). 2. Lipopolysaccharide (LPS) evoked a concentration-dependent generation of GM-CSF from human monocytes. Temporally, this effect was preceded by an increase in GM-CSF mRNA transcripts and abolished by actinomycin D and cycloheximide. 3. LPS-induced GM-CSF release and mRNA expression were associated with a rapid and time-dependent activation of p38 MAP kinase, ERK-1 and ERK-2. 4. The respective MKK-1 and p38 MAP kinase inhibitors, PD 098059 and SB 203580, maximally suppressed LPS-induced GM-CSF generation by >90%, indicating that both of these signalling cascades co-operate in the generation of this cytokine. 5. Electrophoretic mobility shift assays demonstrated that LPS increased nuclear factor kappa B (NF-kappa B) : DNA binding. SN50, an inhibitor of NF-kappa B translocation, abolished LPS-induced NF-kappaB : DNA binding and the elaboration of TNFalpha, a cytokine known to be regulated by NF-kappaB in monocytes. In contrast, SN50 failed to affect the release of GM-CSF from the same monocyte cultures. 6. Collectively, these results suggest that the generation of GM-CSF by LPS-stimulated human monocytes is regulated in a co-operative fashion by p38 MAP kinase- and MKK-1-dependent signalling pathways independently of the activation of NF-kappa B.

Indexed as

Enzyme InhibitorsFlavonoidsGranulocyte-Macrophage Colony-Stimulating FactorHumansImidazolesLipopolysaccharidesMAP Kinase Kinase 1Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesMonocytesNF-kappa Bp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesPyridines2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneEnzyme InhibitorsFlavonoidsGranulocyte-Macrophage Colony-Stimulating FactorImidazolesLipopolysaccharidesMAP2K1 protein, humanMAP Kinase Kinase 1Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesPyridinesRNA, MessengerSB 203580Tumor Necrosis Factor-alpha

Identifiers

PMID11082122
PMCPMC1572440
OpenAlexW1998017399

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.