| First Author | Chiba T | Year | 2011 |
| Journal | FEBS Lett | Volume | 585 |
| Issue | 22 | Pages | 3577-81 |
| PubMed ID | 22024480 | Mgi Jnum | J:180263 |
| Mgi Id | MGI:5305914 | Doi | 10.1016/j.febslet.2011.10.024 |
| Citation | Chiba T, et al. (2011) IkappaBL, a novel member of the nuclear IkappaB family, inhibits inflammatory cytokine expression. FEBS Lett 585(22):3577-81 |
| abstractText | We previously reported that IkappaBL prevents experimental autoimmune arthritis. The molecular mechanism, however, still remains unclear. In contrast to four splicing-isoforms of IkappaBL in human, two isoforms were identified in mouse. The major isoform IkappaBL-alpha(S) suppressed LPS-induced NF-kappaB activation and transcription of TNFalpha and IL-6, but not IL-1beta. The suppressive activity required the nuclear localization signal and the ankyrin repeat domain of IkappaBL. IkappaBL did not affect the nuclear translocation of the NF-kappaB dimer. These findings point to IkappaBL as being a novel member of the nuclear IkappaB family, which functions in the nucleus and controls various inflammatory responses including autoimmune arthritis. |
