Journal
CELL
Volume 104, Issue 1, Pages 33-42Publisher
CELL PRESS
DOI: 10.1016/S0092-8674(01)00189-1
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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/lonomycin-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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