-
27浏览
-
0点赞
-
0收藏
-
0分享
-
87下载
-
0评论
-
引用
期刊论文
Antibody-induced engagement of 182 integrins on adherent human neutrophils triggers activation of p21r, through tyrosine phosphorylation of the protooncogene product Vav
Proc. Natl. Acad. Sci. USA Vol. 93, pp. 8431-8436, August 1996,-0001,():
It is known that 132 integrins are crucial for leukocyte cell-cell and cell-matrix interactions, and accumulating evidence now suggests that integrins serve not only as a structural link but also as a signal-transducing unit that controls adhesion-induced changes in cell functions. In the present study, we plated human neutrophils on surface-bound anti-132 (CD18) antibodies and found that the small GTPbinding protein p2lras is activated by 132 integrins. Pretreatment of the cells with genistein, a tyrosine kinase inhibitor, led to a complete block of p21raS activation, an effect that was not achieved with either U73122, which abolishes the 182 integrininduced Ca2+ signal, or wortmannin, which totally inhibits the phosphatidylinositol 3-kinase activity. Western blot analysis revealed that antibody-induced engagement of 132 integrins causes tyrosine phosphorylation of several proteins in the cells. One of these tyrosine-phosphorylated proteins had an apparent molecular mass of 95 kDa and was identified as the protooncogene product Vav, a p2lraS guanine nucleotide exchange factor that is specifically expressed in cells of hematopoietic lineage. A role for Vav in the activation of p2lras is supported by the observations that antibody-induced engagement of 132 integrins causes an association of Vav with p21ras and that the effect of genistein on p2lraS activation coincided with its ability to inhibit both the tyrosine phosphorylation of Vav and the Vav-p21ras association. Taken together, these results indicate that antibody-induced engagement of 132 integrins on neutrophils triggers tyrosine phosphorylation of Vav and, possibly through its association, a downstream activation of p2lras.
【免责声明】以下全部内容由[郑利民]上传于[2009年04月27日 14时30分09秒],版权归原创者所有。本文仅代表作者本人观点,与本网站无关。本网站对文中陈述、观点判断保持中立,不对所包含内容的准确性、可靠性或完整性提供任何明示或暗示的保证。请读者仅作参考,并请自行承担全部责任。
本学者其他成果
同领域成果