IkB« Is a Key Regulator of B Cell Expansion by Providing Negative Feedback on cRel and RelA in a Stimulus-Specific Manner

RelA in a Stimulus - Specific Manner by Providing Negative Feedback on cRel and Is a Key Regulator of B Cell Expansion

RelA in a Stimulus - Specific Manner by Providing Negative Feedback on cRel and Is a Key Regulator of B Cell Expansion ε B κ

Rela in a Stimulus-specific Manner by Providing Negative Feedback on Crel and Is a Key Regulator of B Cell Expansion Ε B Κ I

IκBε is a key regulator of B cell expansion by providing negative feedback on cRel and RelA in a stimulus-specific manner.

The transcription factor NF-κB is a regulator of inflammatory and adaptive immune responses, yet only IκBα was shown to limit NF-κB activation and inflammatory responses. We investigated another negative feedback regulator, IκBε, in the regulation of B cell proliferation and survival. Loss of IκBε resulted in increased B cell proliferation and survival in response to both antigenic and innate s...

IkBb enhances the generation of the low-affinity NFkB/RelA homodimer

The NFkB family of dimeric transcription factors regulate inflammatory and immune responses. While the dynamic control of NFkB dimer activity via the IkB–NFkB signalling module is well understood, there is little information on how specific dimer repertoires are generated from Rel family polypeptides. Here we report the iterative construction—guided by in vitro and in vivo experimentation—of a ...