Abstract
Cell migration is a key event in physiological processes such as embryonic development, tissue repair, angiogenesis and immune responses. Alteration of the migration program is an important component in multiple pathologies, including chronic inflammation, autoimmunity and tumor metastasis. Understanding of the precise mechanisms at the basis of cellular migration may lead to the identification of novel therapeutic approach for these diseases. Recent evidences show that the interplay between the lipid kinases phosphatidylinositol 3-kinase (PI3Ks) and small GTPases play a critical role in driving cell migration. In this review we will describe the role of these molecules and the interaction between their signal cascades in leukocyte polarization and amoeboid migration.
Copyright © 2012 Elsevier Ltd. All rights reserved.
MeSH terms
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Animals
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Cell Movement / genetics
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Cell Movement / immunology
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Cell Movement / physiology
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Chemotactic Factors / genetics
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Chemotactic Factors / metabolism
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Chemotactic Factors / physiology
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Humans
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Immune System Diseases / genetics*
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Immune System Diseases / metabolism
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Leukocyte Disorders / genetics*
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Leukocyte Disorders / metabolism
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Models, Biological
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Monomeric GTP-Binding Proteins / genetics
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Monomeric GTP-Binding Proteins / metabolism
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Monomeric GTP-Binding Proteins / physiology*
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Phosphatidylinositol 3-Kinases / genetics
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Phosphatidylinositol 3-Kinases / metabolism
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Phosphatidylinositol 3-Kinases / physiology*
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Receptors, Chemokine / genetics
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Receptors, Chemokine / metabolism
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Receptors, Chemokine / physiology
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Signal Transduction / genetics
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Signal Transduction / immunology
Substances
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Chemotactic Factors
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Receptors, Chemokine
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Phosphatidylinositol 3-Kinases
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Monomeric GTP-Binding Proteins
Supplementary concepts
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Neutrophil Chemotactic Response, Abnormal