Mitogen-activated protein (MAP) kinase regulates production of tumor necrosis factor-alpha and release of arachidonic acid in mast cells. Indications of communication between p38 and p42 MAP kinases

Aggregation of the high affinity IgE receptor (FcepsilonRI) in a mast cell line resulted in activation of the p42 and the stress-activated p38 mitogen-activated protein (MAP) kinases. Selective inhibition of these respective kinases with PD 098059 and SB 203580 indicated that p42 MAP kinase, but not...

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Bibliographic Details
Published in:The Journal of biological chemistry 1997-05, Vol.272 (20), p.13397-13402
Main Authors: Zhang, C, Baumgartner, R A, Yamada, K, Beaven, M A
Format: Article
Language:English
Subjects:
Animals
Arachidonic Acid - metabolism
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Cell Line
Mast Cells - metabolism
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinases
p38 Mitogen-Activated Protein Kinases
Protein-Tyrosine Kinases - metabolism
Signal Transduction
Tumor Necrosis Factor-alpha - biosynthesis
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Summary:Aggregation of the high affinity IgE receptor (FcepsilonRI) in a mast cell line resulted in activation of the p42 and the stress-activated p38 mitogen-activated protein (MAP) kinases. Selective inhibition of these respective kinases with PD 098059 and SB 203580 indicated that p42 MAP kinase, but not p38 MAP kinase, contributed to the production of the cytokine, tumor necrosis factor-alpha, and the release of arachidonic acid in these cells. Neither kinase, however, was essential for FcepsilonRI-mediated degranulation or constitutive production of tumor growth factor-beta. Studies with SB 203580 and the p38 MAP kinase activator anisomycin also revealed that p38 MAP kinase negatively regulated activation of p42 MAP kinase and the responses mediated by this kinase.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.272.20.13397