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Volume 272, Number 20, Issue of May 16, 1997 pp. 13397-13402
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

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

(Received for publication, December 11, 1996, and in revised form, March 14, 1997)

Cheng Zhang , Rudolf A. Baumgartner , Koji Yamada and Michael A. Beaven

From the Laboratory of Molecular Immunology, NHLBI, National Institutes of Health, Bethesda, Maryland 20892-1760

Aggregation of the high affinity IgE receptor (Fcepsilon RI) 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 Fcepsilon RI-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.


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