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Activation of p38 in Stimulated Human Neutrophils: Phosphorylation of the Oxidase Component p47phoxby p38 and ERK but Not by JNK

https://doi.org/10.1006/abbi.1996.0470Get rights and content

Abstract

Incubation of human neutrophils with FMLP, a chemotactic peptide, or PMA, a stimulator of protein kinase C, resulted in the activation of p38, a proline-directed kinase. Previous studies had shown that extracellular signal-regulated kinase (ERK), another proline-directed kinase, was activated with similar kinetics in neutrophils stimulated with FMLP and PMA (1, 2). Because one possible target for these proline-directed kinases is p47phox, a component of the respiratory burst oxidase, we examined the phosphorylation of this protein by p38 and ERK, as well as JNK, another proline-directed kinase present in neutrophils. We found that both p38 and ERK phosphorylated p47phoxat the same site and at similar rates, but that p47phoxwas not a substrate for JNK. These data show that p38, like ERK, can be activated in neutrophils exposed to an appropriate stimulus, and that some but not all proline-directed kinases are able to participate in the phosphorylation of a protein essential for normal neutrophil function.

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Supported in part by USPHS Grants AI-24227, AI-28479, AI-15136, GM-37696, and RR-00833, by BSRI-4403 from The Ministry of Education of Korea, and by the Stein Endowment Fund. J.E.B. is Chargé de Recherche-1-CNRS and a recipient of a postdoctoral fellowship from the Arthritis Foundation. J.-W.P. is Associate Professor of Biochemistry, Kyungpook University, Taegu, Korea. E.S. is supported by a postdoctoral fellowship from the Deutsche Forschungsgemeinschaft.

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