Darren F. Boehning, Ph.D.

BCB Graduate Program

Description of Research

​Calcium and Cell Death

Our lab is interested in apoptotic cell death, and how this process is altered in cancer and neurodegeneration.  One area of investigation concerns calcium channel activation during apoptosis. The inositol 1,4,5-trisphosphate receptor (IP3R) is a ligand-gated ion channel which releases calcium from ER stores. We and others have shown that the IP3R plays a critical role in apoptotic calcium release. Our current efforts are focused several related projects. One project investigates the molecular mechanisms leading to calcium release from the IP3R in response to activation of the Fas death receptor with relevance to lymphoma and autoimmunity.  Another project is investigating a role for BRCA1, which is mutated in hereditary breast and ovarian cancer, as a pro-apoptotic protein and modulator of IP3R activity.

Cardiovascular Disease

Our lab is interested in how the IP3R calcium channel regulates cardiovascular physiology. Our recent work has focused on how this channel contributes to ventricular cardiomyocyte contractility and the hypertrophic stress response. We are currently evaluating the role of IP3R channels in signaling downstream of endothelin-1 stimulation, and how these channels regulate the complex spatio-temporal aspects of calcium signaling in ventricular cardiomyocytes. Finally, we are interested in how post-translation modifications of proteins with lipids such as palmitic acid regulates cardiomyocyte function, with a focus on G protein-coupled receptor signaling.

Neurodegenerative Diseases

A major focus of our lab is apoptotic signaling in neurodegeneration. We are investigating how the ubiquilin family of proteins contribute to the pathogenesis of Alzheimer’s disease and amyotrophic lateral sclerosis.  Specifically, we have evidence that the ubiquilin proteins function as molecular chaperones in neurons preventing the aggregation of disease-relevant proteins. We are investigating how the activity of these proteins is altered during disease progression to affect neuronal proteostasis.

Contact Information


Department of Biochemistry and Molecular Biology

University of Texas Health Science Center at Houston

6431 Fannin, Suite 6.161

Houston, TX, 77030

Office: 713-500-6167   Lab: 713-500-6163


Ph.D. - Thomas Jefferson University

Postdoctoral Fellow - Johns Hopkins University

Research Interests

Cancer, Neurodegeneration, Apoptosis, Cell Death, Calcium Signaling, Inositol 1,4,5-Trisphosphate Receptors, Death Receptors

© Copyright 2008-Present - The University of Texas Health Science Center at Houston (UTHealth)