Evidence map›Paper›PMID 11274363›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Role of MEKK2-MEK5 in the regulation of TNF-alpha gene expression and MEKK2-MKK7 in the activation of c-Jun N-terminal kinase in mast cells.

K Chayama, P J Papst, T P Garrington, J C Pratt, T Ishizuka, S Webb, S Ganiatsas, L I Zon, W Sun, G L Johnson and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 70 citations in OpenAlex.

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  11. Assessing developmental roles of MKK4 and MKK7 in vitro.Communicative & integrative biology · 2012
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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

11 authors at 4 institutions in 1 country.

K ChayamaDivision of Basic Sciences, Department of Pediatrics, and the Program in Molecular Signal Transduction, National Jewish Medical and Research Center, Denver, CO 80206, USA.
P J Papst
T P Garrington
J C Pratt
T Ishizuka
S Webb
S Ganiatsas
L I Zon
W Sun
G L Johnson
E W Gelfand
National Jewish Health · USUniversity of Colorado Denver · USUniversity of Colorado Health · USHoward Hughes Medical Institute · US

Funding

REGULATION OF SEQUENTIAL PROTEIN KINASE PATHWAYSR01DK037871 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JOHNSON, GARY L. · 1986 to 2011
$3.7M
REGULATION OF MAST CELL CYTOKINE PRODUCTIONR01AI042246 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 1998 to 2002
$826k
MEKK2 Regulation of Mast Cell/T Cell Cytokine ProductionR21AI042246 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 2003 to 2003
$283k
NIAID NIH HHS AI-42246NIDDK NIH HHS DK-37871NIDDK NIH HHS R01 DK037871
6 · The paper itself

Abstract

Cross-linking of the high-affinity IgE receptor (FcepsilonRI) on mast cells with IgE and multivalent antigen triggers mitogen-activated protein (MAP) kinase activation and cytokine gene expression. We report here that MAP kinase kinase 4 (MKK4) gene disruption does not affect either MAP kinase activation or cytokine gene expression in response to cross-linking of FcepsilonRI in embryonic stem cell-derived mast cells. MKK7 is activated in response to cross-linking of FcepsilonRI, and this activation is inhibited by MAP/ERK kinase (MEK) kinase 2 (MEKK2) gene disruption. In addition, expression of kinase-inactive MKK7 in the murine mast cell line MC/9 inhibits c-Jun NH(2)-terminal kinase (JNK) activation in response to cross-linking of FcepsilonRI, whereas expression of kinase-inactive MKK4 does not affect JNK activation by this stimulus. However, FcepsilonRI-induced activation of the tumor necrosis factor-alpha (TNF-alpha) gene promoter is not affected by expression of kinase-inactive MKK7. We describe an alternative pathway by which MEKK2 activates MEK5 and big MAP kinase1/extracellular signal-regulated kinase 5 in addition to MKK7 and JNK, and interruption of this pathway inhibits TNF-alpha promoter activation. These findings suggest that JNK activation by antigen cross-linking is dependent on the MEKK2-MKK7 pathway, and cytokine production in mast cells is regulated in part by the signaling complex MEKK2-MEK5-ERK5.

Indexed as

Cell LineEnzyme ActivationGene Expression RegulationJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 5MAP Kinase Kinase 7MAP Kinase Kinase Kinase 2MAP Kinase Kinase KinasesMast CellsMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPromoter Regions, GeneticTumor Necrosis Factor-alphaJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 5MAP Kinase Kinase 7MAP Kinase Kinase Kinase 2MAP Kinase Kinase KinasesMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesTumor Necrosis Factor-alpha

Identifiers

PMID11274363
PMCPMC31880
OpenAlexW1977906224

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.