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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Agammaglobulinaemia Tyrosine Kinase
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Agammaglobulinemia / enzymology
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Animals
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B-Lymphocytes / metabolism
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Blotting, Western
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Cell Line
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Chickens
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Enzyme Activation / physiology
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Humans
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Isoenzymes / deficiency
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Isoenzymes / genetics
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Isoenzymes / metabolism*
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Mitogen-Activated Protein Kinase 8
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Mitogen-Activated Protein Kinases / metabolism*
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Phospholipase C gamma
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Precipitin Tests
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Protein-Tyrosine Kinases / deficiency
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Protein-Tyrosine Kinases / genetics
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Protein-Tyrosine Kinases / metabolism*
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Receptors, Antigen, B-Cell / metabolism*
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Signal Transduction / physiology
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Transfection
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Type C Phospholipases / deficiency
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Type C Phospholipases / genetics
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Type C Phospholipases / metabolism*
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rac1 GTP-Binding Protein / metabolism*
Substances
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Isoenzymes
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Receptors, Antigen, B-Cell
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Protein-Tyrosine Kinases
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Agammaglobulinaemia Tyrosine Kinase
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BTK protein, human
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Mitogen-Activated Protein Kinase 8
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Mitogen-Activated Protein Kinases
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Type C Phospholipases
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Phospholipase C gamma
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rac1 GTP-Binding Protein