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ID 25926
本文ファイル
著者
Inoue, Kazumi
キーワード
Akt
Fcγreceptor
Phagocytosis
Phosphoinositide 3-kinase
PKCδ
NDC
医学
抄録(英)
Stimulation of macrophages by various ligands results in the activation of both phosphoinositide 3-kinase (PI3K) and protein kinase C (PKC). Here, we showed that PKCδ selectively inhibits class IA PI3K. Prior exposure of macrophages to a PKC activator, phorbol 12-myristate 13-acetate (PMA) inhibited the PI3K activation induced by the Fcγ receptor (FcγR) ligation but not that induced by C5a. Prolonged PKC inhibition by GF109203X increased the basal PI3K activity of quiescent macrophages. The effect of the PKC inhibitor can be observed in macrophages from mice lacking class IB PI3K (p110γ). Thus PKC was suggested to selectively attenuate the class IA activity. Chronic PKC activation by PMA induced PKCδ degradation and Akt activation. Enhancement of the basal Akt actvity was also observed in cells stably deficient in PKCδ prepared by shRNA technique. FcγR-mediated phagocytosis was dramatically increased in these cells. Thus it is suggested that inactivation of class IA PI3K by PKCδ is functioning in regulation of FcγR-mediated phagocytosis.
掲載誌名
The Journal of Biochemistry
145巻
1号
開始ページ
87
終了ページ
94
出版年月日
2009
出版者
Other Oxford University Press
ISSN
0021-924X
NCID
出版者DOI
言語
英語
NII資源タイプ
学術雑誌論文
広大資料タイプ
学術雑誌論文
DCMIタイプ
text
フォーマット
application/pdf
著者版フラグ
author
権利情報
Copyright (c) 2008 The Japanese Biochemical Society
関連情報URL
部局名
医歯薬学総合研究科