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

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.

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