Class-ⅠA Phosphoinositide 3-Kinase p110β Triggers GPCR-Induced Superoxide Production in p110γ-Deficient Murine Neutrophils
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- Nigorikawa Kiyomi
- Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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- Hazeki Kaoru
- Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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- Kumazawa Takashi
- Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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- Itoh Yuhta
- Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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- Hoshi Megumi
- Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
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- Hazeki Osamu
- Department of Physiological Chemistry, Graduate School of Biomedical & Health Sciences, Hiroshima University, Japan
書誌事項
- タイトル別名
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- Class-IA Phosphoinositide 3-Kinase p110<I>β</I> Triggers GPCR-Induced Superoxide Production in p110<I>γ</I>-Deficient Murine Neutrophils
- Class-IA Phosphoinositide 3-Kinase p110^|^beta; Triggers GPCR-Induced Superoxide Production in p110^|^gamma;-Deficient Murine Neutrophils
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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.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 120 (4), 270-279, 2012
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205178927488
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- NII論文ID
- 10031147575
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC3sXktV2n
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 024148615
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- PubMed
- 23149576
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- 使用不可