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Despite the importance of the Vav family proteins for B cell receptor (BCR) signaling, their activation mechanisms remain poorly understood. We demonstrate here that adaptor molecules Grb2 and BLNK, in addition to Vav, are required for efficient Rac1 activation in response to BCR stimulation. Loss of either Grb2 or BLNK results in decreased translocation of Vav3 to membrane rafts. By expression of Vav3 as a raft-targeted construct, the defective Rac1 activation in Grb2- or BLNK-deficient B cells is restored. Hence, our findings suggest that Grb2 and BLNK cooperate to localize Vav into membrane rafts, thereby contributing to optimal activation of Vav in B cells.

Type

Journal article

Journal

Immunity

Publication Date

06/2003

Volume

18

Pages

777 - 787

Keywords

Adaptor Proteins, Signal Transducing, Animals, B-Lymphocytes, Carrier Proteins, Cell Cycle Proteins, Guanine Nucleotide Exchange Factors, Membrane Microdomains, Mice, Phosphoproteins, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-vav, Receptors, Antigen, B-Cell