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Anesthes. 2012;116(4): doi: /ALN.0b013e31824b9512 Figure Legend:

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Presentation on theme: "Anesthes. 2012;116(4): doi: /ALN.0b013e31824b9512 Figure Legend:"— Presentation transcript:

1 From: The μ-Opioid Receptor in Cancer Progression:Is There a Direct Effect?
Anesthes. 2012;116(4): doi: /ALN.0b013e31824b9512 Figure Legend: Fig. 1. Schematic diagram representing the mechanism(s) by which methylnaltrexone inhibits angiogenesis. Vascular endothelial growth factor (VEGF) binding to VEGF receptors induces Src activation, Src-mediated Akt, RhoA, and mammalian target of rapamycin (mTOR) activation and consequent endothelial cell proliferation, migration, and actin cytoskeletal reorganization required for angiogenesis. Methylnaltrexone (MNTX) inhibits the μ-opioid receptor (MOR) and promotes tyrosine phosphatase activity, leading to Src inactivation. This promotes Akt, RhoA, and mTOR inactivation and consequent inhibition of angiogenesis. Date of download: 10/16/2017 Copyright © 2017 American Society of Anesthesiologists. All rights reserved.


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