AI Article Synopsis
- Btk is crucial for B cell development and function, particularly in activating the B cell antigen receptor (BCR) and the JNK1 signaling pathway.
- Recent findings indicate that Btk is necessary for BCR-induced Rac1 activation, which is not impacted by the absence of another protein, PLC-gamma2.
- The study suggests that Btk influences both the Rac1 and PLC-gamma2 pathways, both of which are important for the JNK1 response initiated by BCR activation.
Article 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 NH(2)-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-gamma2 (PLC-gamma2). Since PLC-gamma2 is also required for BCR-mediated JNK1 response, our results suggest that Btk regulates Rac1 pathway as well as PLC-gamma2 pathway, both of which contribute to the BCR-mediated JNK1 response.
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| http://dx.doi.org/10.1016/s0014-5793(02)02375-x | DOI Listing |
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