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The molecular mechanism of B cell activation by toll-like receptor protein RP-105.
Chan, V W; Mecklenbräuker, I; Su, I; Texido, G; Leitges, M; Carsetti, R; Lowell, C A; Rajewsky, K; Miyake, K; Tarakhovsky, A.
Affiliation
  • Chan VW; Department of Laboratory Medicine, University of California, San Francisco, California 94143, USA.
J Exp Med ; 188(1): 93-101, 1998 Jul 06.
Article in En | MEDLINE | ID: mdl-9653087
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.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Membrane Glycoproteins / B-Lymphocytes / Receptors, Cell Surface / Drosophila Proteins Limits: Animals Language: En Journal: J Exp Med Year: 1998 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Membrane Glycoproteins / B-Lymphocytes / Receptors, Cell Surface / Drosophila Proteins Limits: Animals Language: En Journal: J Exp Med Year: 1998 Document type: Article