NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells.

@article{Sasaki2008NIKOA,
  title={NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells.},
  author={Yoshiteru Sasaki and Dinis Pedro Calado and Emmanuel Derudder and Baochun Zhang and Yuri Shimizu and Fabienne Mackay and Shin-ichi Nishikawa and Klaus Rajewsky and Marc Schmidt-Supprian},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2008},
  volume={105 31},
  pages={
          10883-8
        }
}
BAFF-R-dependent activation of the alternative NF-kappaB pathway plays an essential role in mature B cell survival. Mutations leading to overexpression of NIK and deletion of the TRAF3 gene are implicated in human multiple myeloma. We show that overexpression of NIK in mouse B lymphocytes amplifies alternative NF-kappaB activation and peripheral B cell numbers in a BAFF-R-dependent manner, whereas uncoupling NIK from TRAF3-mediated control causes maximal p100 processing and dramatic hyperplasia… CONTINUE READING

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