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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Cbl-b positively regulates Btk-mediated activation of phospholipase C-gamma2 in B cells.

Genetic studies have revealed that Cbl-b plays a negative role in the antigen receptor-mediated proliferation of lymphocytes. However, we show that Cbl-b-deficient DT40 B cells display reduced phospholipase C (PLC)-gamma2 activation and Ca2+ mobilization upon B cell receptor (BCR) stimulation. In addition, the overexpression of Cbl-b in WEHI-231 mouse B cells resulted in the augmentation of BCR-induced Ca2+ mobilization. Cbl-b interacted with PLC-gamma2 and helped the association of PLC-gamma2 with Bruton's tyrosine kinase (Btk), as well as B cell linker protein ( BLNK). Cbl-b was indispensable for Btk-dependent sustained increase in intracellular Ca2+. Both NH(2)-terminal tyrosine kinase-binding domain and COOH-terminal half region of Cbl-b were essential for its association with PLC-gamma2 and the regulation of Ca2+ mobilization. These results demonstrate that Cbl-b positively regulates BCR-mediated Ca2+ signaling, most likely by influencing the Btk/ BLNK/PLC-gamma2 complex formation.[1]


  1. Cbl-b positively regulates Btk-mediated activation of phospholipase C-gamma2 in B cells. Yasuda, T., Tezuka, T., Maeda, A., Inazu, T., Yamanashi, Y., Gu, H., Kurosaki, T., Yamamoto, T. J. Exp. Med. (2002) [Pubmed]
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