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The NF‐κB subunit RelB is known to act either as an activator or repressor of NF‐κB‐dependent gene expression. The RelB–p52 heterodimer, for instance, is the key element of the alternative NF‐κB signaling pathway supporting the expression of a subset of NF‐κB target genes. By contrast, RelB is crucial for the repression of important pro‐inflammatory cytokines like TNFα or interleukin 1β. Despite accumulating...
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