BAFF-induced NEMO-independent processing of NF-κB2 in maturing B cells

By E. Claudio, K. Brown, S. Park, Hong-shan Wang, U. Siebenlist. Nature Immunology, 2002

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NF-κB and the immune response (2006, background): “Not surprisingly, B cells from RelA / , p100 / , p105 / and c-Rel / mice display increased sensitivity to apoptosis and/or decreased survival ex vivo (Grumont et al., 1998; Claudio et al., 2002; Prendes et al., 2003).”
Activation of IKKα target genes depends on recognition of specific κB binding sites by RelB:p52 dimers (2004, background): “In vivo analysis revealed that IKKa activates an alternative NF-kB pathway based on processing of NF-kB2/ p100 and release of RelB:p52 dimers in response to LTa/b trimers (Dejardin et al, 2002) and other TNF family members ( Claudio et al, 2002; Kayagaki et al, 2002).”
Essential role of RelA Ser311 phosphorylation by ζPKC in NF‐κB transcriptional activation (2003, background): “…or B cells with BAFF, the IKKa subunit of the IKK complex phosphorylates p100, triggering its processing and the release of the RelB±p52 complex that now is free to enter the nucleus (Senftleben et al., 2001; Xiao et al., 2001; Claudio et al., 2002; Dejardin et al., 2002; Kayagaki et al., 2002).”