Bcl10 is a positive regulator of antigen receptor-induced activation of NF-kappaB and neural tube closure |
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Authors: | Ruland J Duncan G S Elia A del Barco Barrantes I Nguyen L Plyte S Millar D G Bouchard D Wakeham A Ohashi P S Mak T W |
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Institution: | Amgen Institute, 620 University Avenue, Toronto, Ontario, Canada M5G 2C1. |
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Abstract: | Bcl10, a CARD-containing protein identified from the t(1;14)(p22;q32) breakpoint in MALT lymphomas, has been shown to induce apoptosis and activate NF-kappaB in vitro. We show that one-third of bcl10-/- embryos developed exencephaly, leading to embryonic lethality. Surprisingly, bcl10-/- cells retained susceptibility to various apoptotic stimuli in vivo and in vitro. However, surviving bcl10-/- mice were severely immunodeficient and bcl10-/- lymphocytes are defective in antigen receptor or PMA/Ionomycin-induced activation. Early tyrosine phosphorylation, MAPK and AP-1 activation, and Ca2+ signaling were normal in mutant lymphocytes, but antigen receptor-induced NF-kappaB activation was absent. Thus, Bcl10 functions as a positive regulator of lymphocyte proliferation that specifically connects antigen receptor signaling in B and T cells to NF-kappaB activation. |
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