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- W2079113729 abstract "Activation of toll-like receptors (TLRs) leads to derepression and subsequent activation of inflammatory response genes that play essential roles in innate and acquired immunity. Derepression requires signal-dependent turnover of the nuclear receptor corepressor NCoR from target promoters, but the mechanisms remain poorly understood. Here, we report that TLR4 uses NFκB to deliver IKKɛ to target promoters that contain “integrated circuits” of κB and AP-1 sites, resulting in local phosphorylation of c-Jun and subsequent NCoR clearance. In contrast, TLR2 signaling leads to rapid activation of CaMKII and phosphorylation of the TBLR1 component of NCoR complexes, bypassing the requirement for c-Jun phosphorylation and enabling NCoR clearance from promoters lacking integrated κB elements. Intriguingly, the IKKɛ-dependent clearance pathway is sensitive to transrepression by liver X receptors, while the CaMKII-dependent pathway is not. These findings reveal mechanisms for integration of TLR, calcium, and nuclear receptor signaling pathways that underlie pathogen-specific responses and disease-specific programs of inflammation." @default.
- W2079113729 created "2016-06-24" @default.
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- W2079113729 date "2009-07-01" @default.
- W2079113729 modified "2023-10-16" @default.
- W2079113729 title "Transcriptional Integration of TLR2 and TLR4 Signaling at the NCoR Derepression Checkpoint" @default.
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- W2079113729 doi "https://doi.org/10.1016/j.molcel.2009.05.023" @default.
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