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Journal of Neurotrauma|March 5, 2003
Delayed treatment of hemoglobin neurotoxicityRaymond F Regan, Bret RogersBiochemical and Biophysical Research Communications|April 28, 2004
Heme oxygenase-2 gene deletion increases astrocyte vulnerability to heminJing Chen, Raymond F ReganCurrent Neurovascular Research|September 27, 2005
Increasing expression of heme oxygenase-1 by proteasome inhibition protects astrocytes from heme-mediated oxidative injuryJing Chen, Raymond F ReganJournal of Neurochemistry|September 1, 2007
Time course of increased heme oxygenase activity and expression after experimental intracerebral hemorrhage: correlation with oxidative injuryMai Chen, Raymond F ReganNeurobiology of Disease|May 1, 2007
Astrocyte-specific heme oxygenase-1 hyperexpression attenuates heme-mediated oxidative injuryLuna Benvenisti-Zarom, Raymond F ReganCurrent Pharmaceutical Design|November 2, 2016
Targeting the Nrf2-Heme Oxygenase-1 Axis after Intracerebral HemorrhageJing Chen-Roetling, Raymond F ReganBiochemical and Biophysical Research Communications|September 27, 2006
Effect of heme oxygenase-1 on the vulnerability of astrocytes and neurons to hemoglobinJing Chen-Roetling, Raymond F ReganJournal of Neurochemistry|July 2, 2016
Haptoglobin increases the vulnerability of CD163-expressing neurons to hemoglobinJing Chen-Roetling, Raymond F ReganFree Radical Research|August 6, 2004
The neurotoxic effect of sickle cell hemoglobinGarig M Vanderveldt, Raymond F ReganCurrent Neurovascular Research|August 12, 2008
Hemoglobin neurotoxicity is attenuated by inhibitors of the protein kinase CK2 independent of heme oxygenase activityJing Chen-Roetling, Zhi Li, Raymond F ReganPageof 6