T. C. Irving

Titin-based force regulates cardiac myofilament structures mediating length-dependent activation

The paper investigates how titin-based forces affect cardiac myofilament structures under stretch, supporting the Frank-Starling mechanism.

Fast myosin binding protein C knockout in skeletal muscle alters length-dependent activation and myofilament structure.

This study investigates the effects of MyBP-C knockout in skeletal muscle, finding altered length-dependent activation and myofilament structure, with implications for MyBP-C-related diseases.

Myosin-binding protein C forms C-links and stabilizes OFF states of myosin

This study shows that MyBP-CC1C7 domains form C-links and stabilize myosin OFF states, affecting crossbridge kinetics and sarcomere function.

Right Ventricular Sarcomere Contractile Depression and the Role of Thick Filament Activation in Human Heart Failure with Pulmonary Hypertension

This study identifies contractile deficits in right ventricular myocytes of HFrEF-PH patients, showing reduced calcium-activated tension and altered myosin ATP turnover, with implications for targeted therapies.

Danicamtiv increases myosin recruitment and alters the chemomechanical cross bridge cycle in cardiac muscle

This study investigates how Danicamtiv increases force and alters cardiac muscle contraction kinetics by modulating myosin function and cross bridge dynamics in cardiac tissue.

TWO CLASSES OF MYOSIN INHIBITORS, BLEBBISTATIN AND MAVACAMTEN, STABILIZE β-CARDIAC MYOSIN IN DIFFERENT STRUCTURAL AND FUNCTIONAL STATES

This study compares how two myosin inhibitors, mavacamten and blebbistatin, stabilize myosin in distinct structural and functional states, potentially affecting cardiac function differently.

In vivo x-ray diffraction and simultaneous EMG reveal the time course of myofilament lattice dilation and filament stretch

This study uses in vivo x-ray diffraction and EMG to measure myofilament lattice dilation and filament stretch during Manduca sexta flight, revealing timing and magnitude of changes in lattice spacing and filament stretching.

Mavacamten stabilizes a folded-back sequestered super-relaxed state of β-cardiac myosin

The paper shows that mavacamten stabilizes a folded-back sequestered super-relaxed state of β-cardiac myosin, linking mutations to cardiomyopathy mechanisms.