Donald James DeGracia Ph.D. (ad3351)

University information

Title: Professor
Unit: Physiology
Department: School of Medicine

Contact information

313-577-6745
4116 Scott Hall
Department of Physiology
540 E. Canfield
Detroit, 48202

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 is not accepting students for the 2023-24 academic year.

Post Graduate Training:
  •  1988-93 Research Assistant, Deptartment of Emergency Medicine, Wayne State University
Category Information:
  • Brain ischemia and reperfusion injury
  • Regulation of protein synthesis
  • Stress-mediated translation arrest
  • Unfolded protein response
Donald James DeGracia Ph.D.

Translational Neuroscience Program

Title: Professor
Laboratory Web Site:

 Physiology Profile

Research Interests:

We study the mechanisms of cell death following brain ischemia and reperfusion, focusing on the causes and consequences of reperfusion-induced inhibition of protein synthesis, or translation arrest. This translation arrest appears to be part of the post-ischemic neuronal stress response. We have evaluated classical ribosome biochemistry, intracellular stress responses and most recently began investigating mRNA regulatory mechanisms, including stress granules and HuR granules. The lab is currently funded by the National Institute of Neurological Disorders and Stroke at the NIH.

Disease/Disorder

Brain ischemia and reperfusion injury: stroke, cardiac arrest and resuscitation brain damage.

Species

Rodents

Methods

Molecular biology.

Key Collaborators

Jose Rafols, Ph.D.

Donald James DeGracia Ph.D.

Courses taught by Donald James DeGracia Ph.D.

Fall Term 2024 (future)

Fall Term 2023

Fall Term 2022

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