Evidence map›Paper›PMID 18222647›Full record

ArticleCellular signalling2008

Activation of c-Jun N-terminal kinase (JNK) by widely used specific p38 MAPK inhibitors SB202190 and SB203580: a MLK-3-MKK7-dependent mechanism.

Harish Muniyappa, Kumuda C Das

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 116 citations in OpenAlex.

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  11. Inflammation: Roles in Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022
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  18. Antiproliferative activity exerted by tricyclohexylphosphanegold(I) n-mercaptobenzoate against MCF-7 and A2780 cell lines: the role of p53 signaling pathways.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2021
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  19. Pathogens (Basel, Switzerland) · 2021
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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

2 authors at 1 institution in 1 country.

Harish MuniyappaDepartment of Pathology and the Arkansas Cancer Research Center, University of Arkansas for Medical Sciences, 4301 West Markham, Slot # 845, Little Rock, AR 72205, United States.
Kumuda C Das
University of Arkansas for Medical Sciences · US

Funding

DNA damage signaling in oxygen toxicity in lung cellsR01HL071558 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI DAS, KUMUDA C · 2004 to 2007
$1.1M
NHLBI NIH HHS 7R01 HL071558NHLBI NIH HHS R01 HL071558
6 · The paper itself

Abstract

Mitogen-activated protein kinases (MAPKs) are key signaling molecules that respond to mitogenic stimulation or environmental stress, resulting in the expression of target proteins. c-Jun N-terminal kinase (JNK) and p38 MAPKs are activated by inflammatory cytokines or environmental stress. Specific p38 MAPK inhibitors, such as SB202190 or SB203580, are widely used to dissect p38 MAPK-related signal transduction mechanisms. While using SB202190 to inhibit p38 MAPK-related signaling, we observed that SB202190 treatment could activate JNK. Further experiments showed that treatment of cells with SB202190 could phosphorylate JNK and activating transcription factor 2 (ATF-2), and increased AP-1 DNA binding. Using multiple cell lines and primary endothelial cells, we demonstrated that specific p38 MAPK inhibitors SB202190 or SB203580 induces the activation of the JNK pathway. Further, using with RNA interference and kinase-inactive expression of intermediates of the JNK pathway, we demonstrated SB202190- or SB203580-induced JNK activation is dependent on the MLK-3-MKK4/MKK7-dependent signal transduction pathway. Finally, we demonstrate that treatment of cells with SB202190 or SB203580 induces the phosphorylation and activation of MLK3.

Indexed as

Activating Transcription Factor 2Cell Line, TumorCells, CulturedDose-Response Relationship, DrugEndothelial CellsEnzyme ActivationEnzyme ActivatorsHumansImidazolesJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 7MAP Kinase Kinase KinasesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase Kinase Kinase 11p38 Mitogen-Activated Protein KinasesPhosphorylation4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazoleActivating Transcription Factor 2ATF2 protein, humanEnzyme ActivatorsImidazolesJNK Mitogen-Activated Protein KinasesMAP2K7 protein, humanMAP Kinase Kinase 7MAP Kinase Kinase KinasesMitogen-Activated Protein Kinase Kinase Kinase 11p38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-junPyridinesRNA, Small InterferingSB 203580Transcription Factor AP-1

Identifiers

PMID18222647
PMCPMC2423944
OpenAlexW2052397527

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.