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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Chiba T,Miyashita K,Sugoh T,Warita T,Inoko H,Kimura M,Sato Tdoi
10.1016/j.febslet.2011.10.024subject
Has Abstractpub_date
2011-11-16 00:00:00pages
3577-81issue
22eissn
0014-5793issn
1873-3468pii
S0014-5793(11)00764-2journal_volume
585pub_type
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