BCR (B-cell antigen receptor)-induced Ca2+ signalling is initiated by activation of tyrosine kinases, which in concert with adaptor proteins and lipid kinases regulate PLC (phospholipase C) γ2 activation. Vav and PI3K (phosphoinositide 3-kinase) are required for optimal Ca2+ responses, although it has not been established, in primary B-cells, if both proteins are components of the same pathway. In vitro evidence suggests that binding of the PI3K lipid product PIP3 to Vav pleckstrin homology domain contributes to Vav activation. However, pharmacological inhibition of PI3K by wortmannin or deletion of the p110δ catalytic subunit has no effect on Vav activation in response to BCR engagement, suggesting that this mechanism does not operate in vivo. We also show that PI3K recruitment to phosphorylated-tyrosine-containing complexes is Vav-independent. Taken together with our previous observation that protein kinase B phosphorylation is normal in Vav-deficient B-cells, we suggest that PI3K activation is Vav-independent in response to strong signals delivered by multivalent cross-linking.
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November 2004
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Conference Article|
October 26 2004
BCR activation of PI3K is Vav-independent in murine B cells
E. Vigorito;
E. Vigorito
1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, U.K.
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E. Clayton;
E. Clayton
1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, U.K.
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M. Turner
M. Turner
1
1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, U.K.
1To whom correspondence should be addressed (email martin.turner@bbsrc.ac.uk).
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Publisher: Portland Press Ltd
Received:
June 18 2004
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2004 The Biochemical Society
2004
Biochem Soc Trans (2004) 32 (5): 781–784.
Article history
Received:
June 18 2004
Citation
E. Vigorito, E. Clayton, M. Turner; BCR activation of PI3K is Vav-independent in murine B cells. Biochem Soc Trans 1 November 2004; 32 (5): 781–784. doi: https://doi.org/10.1042/BST0320781
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