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- W2038356088 abstract "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." @default.
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- W2038356088 date "2011-10-20" @default.
- W2038356088 modified "2023-09-23" @default.
- W2038356088 title "IκBL, a novel member of the nuclear IκB family, inhibits inflammatory cytokine expression" @default.
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- W2038356088 doi "https://doi.org/10.1016/j.febslet.2011.10.024" @default.
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