Bruton's tyrosine kinase regulates B cell antigen receptor-mediated JNK1 response through Rac1 and phospholipase C-γ2 activation

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Abstract

Bruton's tyrosine kinase (Btk) is essential for B cell development and B cell antigen receptor (BCR) function. Recent studies have shown that Btk plays an important role in BCR-mediated c-Jun NH2-terminal kinase (JNK) 1 activation; however, the mechanism by which Btk participates in the JNK1 response remains elusive. Here we show that the BCR-mediated Rac1 activation is significantly inhibited by loss of Btk, while this Rac1 activation is not affected by loss of phospholipase C-γ2 (PLC-γ2). Since PLC-γ2 is also required for BCR-mediated JNK1 response, our results suggest that Btk regulates Rac1 pathway as well as PLC-γ2 pathway, both of which contribute to the BCR-mediated JNK1 response. © 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

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Inabe, K., Miyawaki, T., Longnecker, R., Matsukura, H., Tsukada, S., & Kurosaki, T. (2002). Bruton’s tyrosine kinase regulates B cell antigen receptor-mediated JNK1 response through Rac1 and phospholipase C-γ2 activation. FEBS Letters, 514(2–3), 260–262. https://doi.org/10.1016/S0014-5793(02)02375-X

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