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10 April 2018 Mice Lacking RIP3 Kinase are not Protected from Acute Radiation Syndrome
Katherine D. Castle, Andrea R. Daniel, Everett J. Moding, Lixia Luo, Chang-Lung Lee, David G. Kirsch
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Abstract

Exposure to high doses of ionizing radiation can cause lethal injury to normal tissue, thus inducing acute radiation syndrome. Acute radiation syndrome is caused by depletion of bone marrow cells (hematopoietic syndrome) and irreparable damage to the epithelial cells in the gastrointestinal tract (gastrointestinal syndrome). Although radiation initiates apoptosis in the hematopoietic and gastrointestinal compartments within the first few hours after exposure, alternative mechanisms of cell death may contribute to injury in these radiosensitive tissues. In this study, we utilized mice lacking a critical regulator of necroptosis, receptor interacting protein 3 (RIP3) kinase, to characterize the role of RIP3 in normal tissue toxicity after irradiation. Our results suggest that RIP3-mediated signaling is not a critical driver of acute radiation syndrome.

©2018 by Radiation Research Society.
Katherine D. Castle, Andrea R. Daniel, Everett J. Moding, Lixia Luo, Chang-Lung Lee, and David G. Kirsch "Mice Lacking RIP3 Kinase are not Protected from Acute Radiation Syndrome," Radiation Research 189(6), 627-633, (10 April 2018). https://doi.org/10.1667/RR15001.1
Received: 4 December 2017; Accepted: 1 March 2018; Published: 10 April 2018
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