Hope V. Burnham

The paper investigates MYBPHL nonsense mutations, showing they impair sarcomere incorporation, lead to protein degradation, and cause contractile defects in cardiomyocytes.

This study investigates the effects of conditional MyBP-HL loss in mice, showing adult knock-down causes hypertrophy and atrial dysfunction, while conduction system-specific deletion leads to mild hypercontractility.

This study identifies proteolytic degradation of atrial sarcomere proteins as a mechanism underlying contractile defects in atrial fibrillation.