IKKα limits macrophage NF-κB activation and contributes to the resolution of inflammation
By T. Lawrence, M. Bebien, George Y. Liu, V. Nizet, M. Karin. Nature, 2005
622 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/68b11860c97de20d334f3df5a3be741ae91a5f1c
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Citations in the corpus
- Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “Although IKKaAA mice do not develop ‘‘spontaneous’’ inflammation, they develop an exaggerated inflammatory response when challenged with bacteria, fungal cell wall particles, or even immune complexes (Lawrence et al., 2005).”
- Integrating cell-signalling pathways with NF-κB and IKK function (2007, background): “The complexity of these signalling pathways is further illustrated by the diverse consequences of Ser536 phosphorylation which, in addition to enhancing RelA transactivation, can also induce its translocation to the nucleus, independently of IκB degradation, and enhance its proteolytic degradatio”
- Transcriptional regulation via the NF-κB signaling module (2006, background): “Other studies have revealed that the RelA protein itself is inducibly degraded via proteasome-mediated proteolysis (Saccani et al., 2004; Lawrence et al., 2005), enhancing the dynamic capacity of NF-kB promoter interactions.”
- New regulators of NF-κB in inflammation (2008, background): “Intriguingly, however, IKKα-deficient mice show higher inflammatory responses than wild-type mice, which suggests that IKKα has a role in restricting the transcription of some NF-κB-regulated gene”
- Post-translational modifications regulating the activity and function of the nuclear factor kappa B pathway (2006, background): “IKKa also regulates c-Rel turnover (Lawrence et al., 2005), and c-Rel is also subject to ubiquitination between residues 427 and 480 that promotes c-Rel proteolysis (Chen et al., 1998).”
- NF-κB: linking inflammation and immunity to cancer development and progression (2005, background): “Interestingly, in this pathway, especially in macrophages, the IKK-α subunit has a negative-regulatory role by phosphorylating the NF-κB subunits REL-A and REL on sites that accelerate their nuclear turnover, thereby contributing to termination of the NF-κB-mediated gene-induction respons”