Phosphoinositide 3-kinase: a Key Biochemical Signal for Cell Migration in Response to Chemokines

Overview

Journal Immunol Rev

Specialties Allergy & Immunology
General Surgery

Date 2001 Jan 4

PMID 11138779

Citations 42

Authors

Y Sotsios

S G Ward

Affiliations

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Abstract

Chemokines can couple to distinct signalling pathways that have been demonstrated to mediate not only migration, but also cell growth and transcriptional activation. One particular signalling pathway, namely that controlled by the lipid kinase phosphoinositide 3-kinase (PI3K), has been the focus of much attention with respect to its activation by chemokine receptors and the role it plays in regulating cell migration. Identification of PI3K is arguably one of the most exciting recent developments in biochemical signalling. Pharmacological and genetic studies have now convincingly shown that both CC and CXC chemokines stimulate PI3K-dependent chemotaxis of inflammatory cells such as eosinophils, macrophages, neutrophils and T lymphocytes. This review considers the role of specific sub-classes of PI3Ks (e.g. the p85/p110 heterodimer, PI3Kgamma and PI3K-C2alpha) as well as their downstream effector targets in mediating chemokine-stimulated cell migration.

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