Receptor for advanced glycosylation end-product
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Receptor for Advanced Glycation End-Products or Advanced glycosylation end-product (AGE) receptor or RAGE.
Function[edit | edit source]
AGER gene[edit | edit source]
The Advanced Glycosylation End-Products (AGE) Receptor gene is known as AGER.
ME/CFS[edit | edit source]
Notable studies[edit | edit source]
- 2022, Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE) - (Abstract)
See also[edit | edit source]
Learn more[edit | edit source]
References[edit | edit source]
- ↑ https://pubchem.ncbi.nlm.nih.gov/gene/177
- ↑ Gottschalk, Carl G; Peterson, Daniel; Knox, Konstance; Maynard, Marco; Whelan, Ryan J.; Roy, Avik (May 1, 2022). "Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE)". Molecular and Cellular Neuroscience. 120: 103731. doi:10.1016/j.mcn.2022.103731. ISSN 1044-7431.
serum The clear yellowish fluid that remains from blood plasma after clotting factors have been removed by clot formation. (Blood plasma is simply blood that has had its blood cells removed.)
microglia A type of immune cell, called a macrophage, that lives in the brain. For historical reasons, macrophages have different names based on the part of the body that they normally live in. Macrophages that normally live in the blood are called monocytes. Macrophages that normally live in the skin are called Langerhans cells. Macrophages that normally live in the liver are called Kupffer cells. And macrophages that normally live in the central nervous system are called microglia. Microglia were originally classified as glial cells, under the assumption that the cells had a merely structural function, before it was realized that the cells were in fact immune cells. As the "sentinel cells" of the central nervous system, microglia survey their environment for abnormalities such as infection or tissue damage, and then initiate an immune response to fight the infection or repair the tissue damage.
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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history.