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首页> 外文期刊>FEBS Letters >Roles of p38 MAPK, PKC and PI3‐K in the signaling pathways of NADPH oxidase activation and phagocytosis in bovine polymorphonuclear leukocytes
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Roles of p38 MAPK, PKC and PI3‐K in the signaling pathways of NADPH oxidase activation and phagocytosis in bovine polymorphonuclear leukocytes

机译:p38 MAPK,PKC和PI3‐K在牛多形核白细胞NADPH氧化酶激活和吞噬信号通路中的作用

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摘要

>Stimulation of bovine polymorphonuclear leukocytes (PMN) with serum-opsonized zymosan (sOZ) induced the activation of p38 mitogen-activated protein kinase (MAPK), protein kinase C (PKC) and phosphatidylinositol 3-kinase (PI3-K) and sOZ-induced O2 − production was significantly attenuated by their inhibitors (SB203580 for p38 MAPK, GF109203X for PKC and wortmannin for PI3-K). They caused significant attenuation of sOZ-induced phosphorylation of p47phox as well. Flow cytometric analysis, however, revealed that SB203580 and wortmannin attenuated phagocytosis, but GF109203X facilitated it. The results suggest that p38 MAPK and PI3-K participated in both signaling pathways of NADPH oxidase activation (O2 − production) and phagocytosis, and PKC participated in the signaling pathway of NADPH oxidase activation alone.
机译:>用血清调理的酵母聚糖(sOZ)刺激牛多形核白细胞(PMN)诱导了p38丝裂原活化蛋白激酶(MAPK),蛋白激酶C(PKC)和磷脂酰肌醇3-激酶(PI3-K)的活化sOZ诱导的O 2 -的产生被其抑制剂显着减弱(p38 MAPK为SB203580,PKC为GF109203X,PI3​​-K为渥曼青霉素)。它们也引起sOZ诱导的p47phox磷酸化的显着减弱。流式细胞仪分析,但是,发现SB203580和渥曼青霉素减弱吞噬作用,但GF109203X促进了吞噬作用。结果表明p38 MAPK和PI3-K参与了NADPH氧化酶激活(O 2 -产生)和吞噬的信号通路,而PKC参与了NADPH氧化酶激活和吞噬的信号通路。仅NADPH氧化酶激活。

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