We study heart development, adult heart function and skeletal muscle function using model organisms to understand why changes in proteins that surround the cell’s nucleus lead to cardiovascular disease and skeletal muscle disorders.

​Specifically, we use structural biology techniques to reveal how mutations in nuclear envelope proteins affect folding. We combine this with cell biology and biochemistry, to understand the functional consequences of these mutations at cellular and tissue levels. Furthermore, we use physiological approaches for monitoring heart function of model organisms that are engineered to mimic the cardiomyopathy-causing mutations found in patients.

The goal of our research is to use basic biology to uncover new disease mechanisms to benefit basic scientists and patients alike.