Abstract
The ubiquitin-binding endoribonuclease N4BP1 is a critical immunosuppressor, but the mechanism by which it acts to constrain TLR-induced inflammatory cytokine production has remained unclear. In this issue of Immunity, Gitlin et al. find that N4BP1 works in concert with the non-canonical IκB kinase (IKK) to limit activity of the IKK complex.
Original language | English |
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Pages (from-to) | 929-932 |
Number of pages | 4 |
Journal | Immunity |
Volume | 57 |
Issue number | 5 |
DOIs |
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Publication status | Published - 14 May 2024 |