The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses.
By A. Schmidt, Shirley Shidu Yan, S. Yan, David M. Stern. Journal of Clinical Investigation, 2001
1,233 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Endocrinology, Diabetes and Metabolism, Genetics
View Paper: https://www.semanticscholar.org/paper/21bb188fd1b7beed73c18aad7c6a7afde3e2699b
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Citations in the corpus
- Understanding RAGE, the receptor for advanced glycation end products (2005, background): “Therefore, one mechanism by which the RAGE/NF-κB axis might affect mortality in sepsis is by amplifying the expression of both RAGE and other adhesive receptors, such as ICAM-1 and VCAM-1, which, in turn, enhance recruitment of inflammatory cells (Fig.”
- Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes. (2004, background): “Indeed, the expression of RAGE is upregulated at sites of diverse diseases, from atherosclerosis to Alzheimer’s disease and Amyotrophic Lateral Sclerosis [45,53].”
- S100A8 and S100A9 in inflammation and cancer. (2006, background): “glycation end-products (AGEs), high mobility group box 1 (HMGB1; also known as amphoterin), amyloid-b peptide [121,126,127].”
- The Pattern Recognition Receptor (RAGE) Is a Counterreceptor for Leukocyte Integrins (2003, background): “While RAGE is expressed at low levels in normal tissues and the vasculature, the receptor becomes up-regulated wherever its ligands may accumulate (5).”
- Functions of S100 Proteins (2012, background): “However, in a background of inflammation and/or neurodegenerative disorders, which is accompanied by enhanced expression levels of S100B and the S100B receptor, RAGE, in neural and inflammatory cells [7,320-322], S100B acts synergistically with proinflammatory cytokines and, at higher concentrations”
- Para-inflammation in the aging retina. (2009, background): “Ligands for RAGEs include advanced glycation end products (AGEs), b-amyloid, S100/calgranulin, Mac-1, and others (Herold et al., 2007; Schmidt et al., 2001).”