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

Act1, a negative regulator in CD40- and BAFF-mediated B cell survival.

TNF receptor (TNFR) superfamily members, CD40, and BAFFR play critical roles in B cell survival and differentiation. Genetic deficiency in a novel adaptor molecule, Act1, for CD40 and BAFF results in a dramatic increase in peripheral B cells, which culminates in lymphadenopathy and splenomegaly, hypergammaglobulinemia, and autoantibodies. While the B cell-specific Act1 knockout mice displayed a similar phenotype with less severity, the pathology of the Act1-deficient mice was mostly blocked in CD40- Act1 and BAFF- Act1 double knockout mice. CD40- and BAFF-mediated survival is significantly increased in Act1-deficent B cells, with stronger IkappaB phosphorylation, processing of NF-kappaB2 (p100/p52), and activation of JNK, ERK, and p38 pathways, indicating that Act1 negatively regulates CD40- and BAFF-mediated signaling events. These findings demonstrate that Act1 plays an important role in the homeostasis of B cells by attenuating CD40 and BAFFR signaling.[1]

References

  1. Act1, a negative regulator in CD40- and BAFF-mediated B cell survival. Qian, Y., Qin, J., Cui, G., Naramura, M., Snow, E.C., Ware, C.F., Fairchild, R.L., Omori, S.A., Rickert, R.C., Scott, M., Kotzin, B.L., Li, X. Immunity (2004) [Pubmed]
 
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