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Toll样受体蛋白RP-105激活B细胞的分子机制。

The molecular mechanism of B cell activation by toll-like receptor protein RP-105.

作者信息

Chan V W, Mecklenbräuker I, Su I, Texido G, Leitges M, Carsetti R, Lowell C A, Rajewsky K, Miyake K, Tarakhovsky A

机构信息

Department of Laboratory Medicine, University of California, San Francisco, California 94143, USA.

出版信息

J Exp Med. 1998 Jul 6;188(1):93-101. doi: 10.1084/jem.188.1.93.

Abstract

The B cell-specific transmembrane protein RP-105 belongs to the family of Drosophila toll-like proteins which are likely to trigger innate immune responses in mice and man. Here we demonstrate that the Src-family protein tyrosine kinase Lyn, protein kinase C beta I/II (PKCbetaI/II), and Erk2-specific mitogen-activated protein (MAP) kinase kinase (MEK) are essential and probably functionally connected elements of the RP-105-mediated signaling cascade in B cells. We also find that negative regulation of RP-105-mediated activation of MAP kinases by membrane immunoglobulin may account for the phenomenon of antigen receptor-mediated arrest of RP-105-mediated B cell proliferation.

摘要

B细胞特异性跨膜蛋白RP-105属于果蝇Toll样蛋白家族,这类蛋白可能在小鼠和人类中触发先天免疫反应。在此我们证明,Src家族蛋白酪氨酸激酶Lyn、蛋白激酶CβI/II(PKCβI/II)以及Erk2特异性丝裂原活化蛋白(MAP)激酶激酶(MEK)是B细胞中RP-105介导的信号级联反应的必需且可能功能相关的元件。我们还发现,膜免疫球蛋白对RP-105介导的MAP激酶激活的负调控可能解释了抗原受体介导的RP-105介导的B细胞增殖停滞现象。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d80/2525555/7b6c1b025096/JEM980500.f1.jpg

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