We previously reported that IκBL prevents experimental autoimmune arthritis. The molecular mechanism, however, still remains unclear. In contrast to four splicing-isoforms of IκBL in human, two isoforms were identified in mouse. The major isoform IκBL-α(S) suppressed LPS-induced NF-κB activation and transcription of TNFα and IL-6, but not IL-1β. The suppressive activity required the nuclear localization signal and the ankyrin repeat domain of IκBL. IκBL did not affect the nuclear translocation of the NF-κB dimer. These findings point to IκBL as being a novel member of the nuclear IκB family, which functions in the nucleus and controls various inflammatory responses including autoimmune arthritis. © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Chiba, T., Miyashita, K., Sugoh, T., Warita, T., Inoko, H., Kimura, M., & Sato, T. (2011). IκBL, a novel member of the nuclear IκB family, inhibits inflammatory cytokine expression. FEBS Letters, 585(22), 3577–3581. https://doi.org/10.1016/j.febslet.2011.10.024