Possible new role for NF-κB in the resolution of inflammation
By T. Lawrence, D. Gilroy, P. Colville-Nash, D. Willoughby. Nature Medicine, 2001
724 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/7a0cce796ec44d19671f1964aeb5defcbf964ebc
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Citations in the corpus
- Chronic infantile neurological cutaneous and articular syndrome is caused by mutations in CIAS1, a gene highly expressed in polymorphonuclear cells and chondrocytes. (2002, background): “This hypothesis would be in agreement with the in vivo model of rat carageenin-induced acute inflammation, in which inhibition of NK-k B during the resolution of in-flammation protracts inflammatory responses and prevents apoptosis (Lawrence et al. 2001).”
- Antioxidant and Anti‐Inflammatory Properties of the Citrus Flavonoids Hesperidin and Hesperetin: An Updated Review of their Molecular Mechanisms and Experimental Models (2015, background): “Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a transcription factor that plays a pivotal role in the expression of iNOS, COX-2, TNF-α, and IL-6, which include the NF-κB binding sites in their promoters (Kang et al., 2011; Lawrence et al., 2001).”
- Neuroinflammation in Parkinson’s disease: its role in neuronal death and implications for therapeutic intervention (2009, background): “In the anti-inflammatory phase of inflammation, NFκB promotes apoptosis and expression of mediators such as TGFβ1 and cyclopentenone prostaglandins as well as transcription of genes such as Bax and p53 (Lawrence et al., 2001).”
- Pro-Resolving lipid mediators and Mechanisms in the resolution of acute inflammation (2014, background): “…and chemokine expression (Gilroy et al., 2003; Pasceri et al., 2000); regulate macrophage activation and pro-inflammatory gene expression (Lawrence, 2002); and induce leukocyte apoptosis through a caspase-dependent mechanism (Bishop-Bailey and Hla, 1999; Gilroy et al., 2003; Lawrence et al., 2001).”
- Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox? (2016, neutral): “There are no competing interests to declare.”