Donald James DeGracia Ph.D. (ad3351)

Donald James DeGracia Ph.D. (ad3351)

University Information

Title: Professor
Unit: Physiology
Department: School of Medicine

Contact Information

4116 Scott Hall
Department of Physiology
540 E. Canfield
Detroit, 48202

Office for Teaching & Learning

Title: Associate Professor
Department: Physiology


Office Address: 4116 Scott Hall
Phone: 313-577-6745
Fax: 313-577-5494
Position Title: Professor
Joint Appointments: Center for Molecular Medicine and Genetics
Areas of Interest: Brain ischemia and reperfusion injury, translation, stress granules, ribonomics
Narrative Bio:

Dr. DeGracia studies the mechanisms of cell death following brain ischemia and reperfusion. This clinically relevant research models brain injury that occurs following stroke or following resuscitation from cardiac arrest. The main focus of this work is the causes and consequences of reperfusion-induced inhibition of protein synthesis. Dr. DeGracia's previous work established that phosphorylation of eukaryotic initiation factor 2 alpha occurs in the reperfused brain. Further, this phosphorylation is caused by the eIF2 alpha kinase PERK. PERK activation is part of an endoplasmic reticulum stress response known as the unfolded protein response (UPR). Dr. DeGracia has investigated expression of the UPR in the reperfused brain and developed evidence that the UPR is expressed in an apparently dysfunctional fashion.  Current work in the lab is assessing the role of mRNA regulation via stress granules and HuR granules in prolonged translation arrested in reperfused vulnerable neurons.

Dr. DeGracia's lab is funded by the NIH.

Laboratory Web Site:


Publications are available for download on my laboratory web site.

Post Graduate Training:
  •  1988-93 Research Assistant, Deptartment of Emergency Medicine, Wayne State University
Awards & Honors:

Member, NOMD Study Section at National Institute of Neurological Disorders and Stroke at NIH. 2005 -2008.  Ad hoc, 2009.  Ad hoc ARRA reviewer for NINDS

Category Information:
  • Brain ischemia and reperfusion injury
  • Regulation of protein synthesis
  • Stress-mediated translation arrest
  • Unfolded protein response

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