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. 2017 Sep;12(9):1381–1389. doi: 10.4103/1673-5374.215240

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Copyright: © Neural Regeneration Research

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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Pathways involved in EpoR activation.

Principal signal pathways activated to induce neuroprotection when Epo interacts with EpoR or EpoRβ (expressed in CNS) in response to hypoxia or different types of stress, such as ischemic brain events or inflammation induced by Alzheimer′s disease. Epo or EPO: Erythropoietin; EpoR: Epo receptor; CNS: central nervous system; HiF-1: hypoxia inducible factor; Aβ: beta amyloid peptide; ATP: adenosine triphosphate; JAK: Janus kinase; ROS: reactive oxygen species; GSK-3β: glycogen synthase kinase 3 beta; AKT: protein kinase B; PI3K: phosphoinositol 3′-kinase; STAT5: signal transducer and activator of transcription 5; MeK-1: mitogen-activated protein kinase kinase; Erk1,2: extracellular-regulated kinases 1,2; Bcl2: B-cell lymphoma 2; BclxL: B-cell lymphoma-extra large.