Benjamin Prosser, PhD

Assistant Professor Of Physiology

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705 Clinical Research Building

415 Curie Boulevard

Philadelphia, PA 19104

215-746-1488

Fax: 215-573-2273

bpros@mail.med.upenn.edu

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Faculty Spotlight


January 2015

Benjamin Prosser, PhD

Benjamin Prosser, Ph.D. is a newly appointed Assistant Professor of Physiology. During his graduate and post-doctoral training, Ben investigated the mechanistic underpinnings of key problems in muscle physiology. His work has bridged several disciplines, departments and institutes, including physiology, cell biology, cardiovascular research, biophysics and engineering. He is an emerging leader in new, exciting aspects of the molecular physiology of cardiomyocyte function and signaling; with strong relevance for understanding basic mechanisms of cardiac function, with clear translational implications. Additionally, to achieve his research goals, he is developing and utilizing state-of-the-art imaging, as well as biophysical and biochemical technologies.

In Ben’s Ph.D. work, he made exciting discoveries about the role of the calcium binding protein S100A1 in the regulation of skeletal muscle excitation-contraction coupling. He used unique biochemical approaches, technically-difficult combined single cell electrophysiology, and optical imaging to demonstrate the molecular basis of the binding of S100A1 to the ryanodine receptor Ca2+ release channel, and its functional consequences; ranging from tissue to molecular levels.

His focus switched to cardiac myocytes in his post-doctoral studies. To examine the relationship between Ca2+ signals and force production he invented a novel, cellular glue (MyoTak). MyoTak enabled him to apply precisely controlled stretch to single myocytes fibers, while simultaneously recording tension, Ca2+ signals, and electrophysiological properties. Ben discovered that stretch, Ca2+ signaling, and myocyte functions are intimately interconnected because stretch causes local reactive oxygen species (ROS) generation. ROS generation has rapid and reversible effects on the Ca2+ release channel. Ben discovered the source of the ROS – Nox2, and he has now become famous for discovering X-ROS signaling. His work was published in Science, and comments on its significance are found in many leading journals.

Ben subsequently discovered the relevance of X-ROS signaling for excitation-contraction coupling in skeletal muscle, published in Science Signaling. Notably, he demonstrated its significance in a mouse model of muscular dystrophy, showing that Ben approaches important biological problems from a biophysical perspective; while keeping a bigger picture in mind and being aware of possible connections to clinical issues.

Ben is becoming an actively involved citizen at Penn and has played a major role in bringing super-resolution microscopy to the Perelman School of Medicine. In addition, he participates as a member of the Pennsylvania Muscle Institute and he is involved in graduate student recruiting efforts as a member of the Cell and Molecular Biology graduate group.

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