A Novel ER Stress-Independent Function of the UPR in Angiogenesis

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A Novel ER Stress-Independent Function of the UPR in Angiogenesis Hery Urra, Claudio Hetz Molecular Cell Volume 54, Issue 4, Pages 542-544 (May 2014) DOI: 10.1016/j.molcel.2014.05.013 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 An Interconnection between VEGF Signaling and the Unfolded Protein Response in the Control of Endothelial Cell Survival and Angiogenesis (A) ER stress sensors IRE1α, PERK, and ATF6 have distinct roles in cancer, mediating tumor growth and cell survival. The hypoxic conditions in solid tumors engage the UPR and HIF-1α, a phenomenon required for angiogenesis. (B) VEGF signaling engages the activation of UPR stress sensors in endothelial cells through PLCγ and mTORC1. ATF6 and PERK are required to drive endothelial cell survival and angiogenesis, possibly through a mechanism involving phosphorylation of AKT by the mTORC2 complex and other effects. Molecular Cell 2014 54, 542-544DOI: (10.1016/j.molcel.2014.05.013) Copyright © 2014 Elsevier Inc. Terms and Conditions