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Darren Boehning, PhD

A headshot photo featuring Darren Boehning, PhD, head and assistant dean for research at CMSRU.Administrative Head & Assistant Dean for Research
Professor of Biomedical Sciences

Dr. Boehning received his Bachelor of Science in Molecular Biology from Syracuse University in 1994. In 2001 he obtained his Ph.D. in Cell Biology from Thomas Jefferson University, where he was a Foerderer Fellow examining the function of IP3 receptor calcium channels. His work was recognized with the Alumni Thesis Award for the top thesis of his graduating year. From 2001-2004 he was a post-doctoral fellow in the laboratory of Sol Snyder in the Department of Neuroscience at Johns Hopkins University. His post-doctoral work on gaseous neurotransmission and neuronal cell death was funded by an individual Ruth L. Kirschstein NRSA post-doctoral fellowship from the National Institutes of Health (NIH). From 2005-2013, he was faculty in the Department of Neuroscience and Cell Biology at the University of Texas Medical Branch (UTMB) in Galveston. At UTMB he was director of the Cell Biology Graduate Program. During this time, he was the recipient of multiple NIH grants and was awarded the Distinguished Faculty Teaching Award, the Student Faculty Advocacy Award, and the Excellence in Teaching Award in Cell Biology. From 2013-2019 Dr. Boehning was a faculty member in the Department of Biochemistry and Molecular Biology at the McGovern Medical School at UTHealth. While at UTHealth he served as director of the Graduate Program in Biochemistry and Molecular Biology (2015-2017) and founding director of a new graduate program in Biochemistry and Cell Biology (2017-2018). At UTHealth Dr. Boehning received the Dean’s Teaching Excellence Award (2015-19), the Biochemistry and Cell Biology Outstanding Faculty Award (2018), and served as the GSBS Faculty Marshal of the UTHealth/MD Anderson Commencement (2016)

Dr. Boehning is known for his work on cell death in health and disease. In particular, his work has illustrated the central role of the IP3 receptor calcium channel in mediating apoptotic cell death. He found that the IP3 receptor is essential to the progression of most cell death paradigms, and how this channel is activated during disease. Of note, he discovered how this receptor contributes to apoptotic resistance in lymphoma and other cancers. His basic science approaches have also developed new therapeutic agents for inhibiting cell death by blocking IP3 receptor activity. Finally, in collaboration with clinicians he has shown in laboratory models and in human patients that increased IP3 receptor activity after traumatic injury leads to systemic inflammation and type II diabetes (so called “stress-induced diabetes”) which contributes to morbidity and mortality. These “bench to bedside” approaches may lead to new therapeutics for improving patient survival.