| Class-IA Phosphoinositide 3-Kinase p110β Triggers GPCR-Induced Superoxide Production in p110γ-Deficient Murine Neutrophils. | |
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MedLine Citation:
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PMID: 23149576 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Studies with knockout mice have indicated that the only isoform of phosphoinositide 3-kinase (PI3K) functioning in the oxidative burst of mouse neutrophils in response to heterotrimeric guanine nucleotide-binding protein-coupled receptor (GPCR) agonists is a class-IB PI3K, p110γ. In the present study, we observed that the cells from p110γ(-/-) mice gain a response to N-formyl-Met-Leu-Phe (fMLP) after priming with cytochalasin E. Even the unprimed cells, which show no response to fMLP, produce a significant amount of superoxide, when an effective agonist of the mouse-type fMLP receptors, Trp-Lys-Tyr-Met-Val-D-Met, is used to stimulate the cells. These results suggested that the class-IA isoforms (p110α, p110β, and p110δ) of PI3K are sufficient to trigger and maintain superoxide production. Examination of the effects of isoform-specific inhibitors suggested that the p110β isoform is the primary PI3K triggering the response to GPCR agonists when p110γ is absent. |
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Authors:
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Kiyomi Nigorikawa; Kaoru Hazeki; Takashi Kumazawa; Yuhta Itoh; Megumi Hoshi; Osamu Hazeki |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-11-13 |
Journal Detail:
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Title: Journal of pharmacological sciences Volume: - ISSN: 1347-8648 ISO Abbreviation: J. Pharmacol. Sci. Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-11-14 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101167001 Medline TA: J Pharmacol Sci Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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