DGK味 is involved in LPS-activated phagocytosis through IQGAP1/Rac1 pathway

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• 作者：Masashi Okada^a ; ^{m-okada@med.id.yamagata-u.ac.jp} ; Yasukazu Hozumi^a ; Kiyoshi Iwazaki^a ; Kentaro Misaki^b ; Mitsuaki Yanagida^b ; Yoshihiko Araki^b ; Takashi Watanabe^c ; Hitoshi Yagisawa^d ; Matthew K. Topham^e ; Kozo Kaibuchi^c ; Kaoru Goto^a ; ^{kgoto@med.id.yamagata-u.ac.jp}
• 关键词：Diacylglycerol kinase ; IQGAP ; Rac1 ; Macrophage ; Phagocytosis
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：6 April, 2012
• 卷：420
• 期：2
• 页码：479-484
• 文件大小：683 K

摘要

Diacylglycerol kinase (DGK) plays an important role in phosphoinositide signaling cascade by regulating the intracellular level of diacylglycerol and phosphatidic acid. The DGK family is involved in various pathophysiological responses that are mediated through unique binding partners in different tissues and cells. In this study, we identified a small GTPase effector protein, IQGAP1, as a novel DGK味-associated complex protein. A bacterial endotoxin, lipopolysaccharide (LPS), facilitated the complex formation in macrophages. Both proteins co-localized at the edge and phagocytic cup of the cell. Furthermore, RNA interference-mediated knockdown of DGK味 or IQGAP1 impaired LPS-induced Rac1 activation. Primary macrophages derived from DGK味^{鈭?鈭?/sup> mice attenuated LPS-induced phagocytosis of bacteria. These results suggest that DGK味 is involved in IQGAP1/Rac1-mediated phagocytosis upon LPS stimulation in macrophages.}