Regulation of Vav localization in membrane rafts by adaptor molecules Grb2 and BLNK

54Citations
Citations of this article
33Readers
Mendeley users who have this article in their library.

Abstract

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.

Cite

CITATION STYLE

APA

Johmura, S., Oh-hora, M., Inabe, K., Nishikawa, Y., Hayashi, K., Vigorito, E., … Kurosaki, T. (2003). Regulation of Vav localization in membrane rafts by adaptor molecules Grb2 and BLNK. Immunity, 18(6), 777–787. https://doi.org/10.1016/S1074-7613(03)00139-0

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free