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When most people think of calcium, they think of the building blocks of bone. However, all of the cells in your body use calcium as a way to transmit signals from the outside of the cell to the inside. Sometimes this can result in the death of the cell. This is a normal process that is happening all of the time in your body to remove old cells and those which are no longer needed. Sometimes, this process goes awry leading to cancer (not enough cell death) or neurodegeneration (too much cell death). We try to understand how this happens and what we can do to prevent diseases associated with altered cell death.

Our Work In Scientific Terms

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 that 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 on 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.  Most of our efforts are currently focused on how protein S-acylation regulates T cell signaling, with a special emphasis on the acylating and deacylating enzymes.



Heart disease is responsible for 25% of all deaths in the United States. When the heart is overworked there are often changes in how the heart functions. For example, in people with high blood pressure, the cells of the heart get bigger to try to help it pump with greater force. However, these changes also increase the risk of heart failure. We try to understand how pathological changes in the heart occur at the molecular level, and whether these processes can be reversed in people with heart disease.

Our Work In Scientific Terms

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 have previously evaluated 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. We are currently 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 such as Alzheimer's disease and Lou Gehrig's disease (also known as ALS) are devastating and fatal diseases with few treatment options. A common theme in many neurodegenerative diseases is that proteins in the neurons clump up and become toxic causing them to die. We study a protein called ubiquilin which may help to stop other proteins from clumping up and thus prevent neurons from dying. We are currently studying how these proteins are associated with Alzheimer's disease and ALS, and whether increasing the activity of ubiquilin can slow or prevent disease.

Our Work In Scientific Terms

A past focus of our lab was apoptotic signaling in neurodegeneration. We investigated how the ubiquilin family of proteins contributed to the pathogenesis of Alzheimer’s disease and more recently amyotrophic lateral sclerosis (ALS).  Specifically, we published evidence that the ubiquilin family of proteins function as molecular chaperones in neurons preventing the aggregation of disease-relevant proteins. We still have an interest in investigating how the mutations in the ubiquilin-2 gene (UBQLN2) contributes to disease progression of ALS. 

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