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Publication : Bcl10 is a positive regulator of antigen receptor-induced activation of NF-kappaB and neural tube closure.

First Author  Ruland J Year  2001
Journal  Cell Volume  104
Issue  1 Pages  33-42
PubMed ID  11163238 Mgi Jnum  J:67297
Mgi Id  MGI:1930354 Doi  10.1016/s0092-8674(01)00189-1
Citation  Ruland J, et al. (2001) Bcl10 is a positive regulator of antigen receptor-induced activation of NF-kappaB and neural tube closure. Cell 104(1):33-42
abstractText  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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