Abstract
IL-2 and IL-4 induce proliferation of TS1 alpha beta cells. Activation of the zeta isoform of protein kinase C is an important step in IL-2-, but not IL-4-mediated proliferation. In addition, protein kinase C-zeta is implicated in IL-2-mediated actin organization. Given the established involvement of the Rho family of small guanine nucleotide-binding proteins in organization of actin structures, we analyze the possible relationships between Rho and protein kinase C-zeta. Using the Rho-like protein family-specific toxin B from Clostridium difficile, we report in this work that IL-2, but not IL-4, induces a Rho-dependent activation of protein kinase C-zeta. This signaling event is mediated by the activation of phosphatidylinositol 3-kinase. In contrast, IL-4 induces a Rho-independent, phosphatidylinositol 3-kinase-mediated activation of protein kinase C-zeta, but this pathway has no implications in cytoskeleton organization.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / drug effects
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Actins / immunology
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Actins / metabolism*
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Animals
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Bacterial Proteins*
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Bacterial Toxins / pharmacology
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Cell Line
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Clostridioides difficile / immunology
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Enzyme Activation / immunology
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GTP-Binding Proteins / physiology*
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Humans
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Interleukin-2 / physiology*
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Interleukin-4 / pharmacology
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Lymphocyte Activation / drug effects
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Mice
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Phosphatidylinositol 3-Kinases
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Phosphotransferases (Alcohol Group Acceptor) / antagonists & inhibitors
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Phosphotransferases (Alcohol Group Acceptor) / metabolism
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Phosphotransferases (Alcohol Group Acceptor) / physiology*
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Protein Kinase C / antagonists & inhibitors
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Protein Kinase C / metabolism
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Protein Kinase C / physiology*
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Signal Transduction / immunology
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T-Lymphocytes / immunology
Substances
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Actins
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Bacterial Proteins
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Bacterial Toxins
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Interleukin-2
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toxB protein, Clostridium difficile
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Interleukin-4
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Phosphotransferases (Alcohol Group Acceptor)
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Protein Kinase C
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GTP-Binding Proteins