Myopathy Archives

The increase in non-cross-bridge forces after stretch of activated striated muscle is related to titin isoforms.

Effect of levosimendan on the contractility of muscle fibers from nemaline myopathy patients with mutations in the nebulin gene.

Pompe disease results in a Golgi-based glycosylation deficit in human induced pluripotent stem cell-derived cardiomyocytes.

Alterations at the Cross-Bridge Level Are Associated with a Paradoxical Gain of Muscle Function In Vivo in a Mouse Model of Nemaline Myopathy.

Muscle histopathology in nebulin-related nemaline myopathy: ultrastrastructural findings correlated to disease severity and genotype.

Large-Scale Modulation of Titin Elasticity by S-Glutathionylation of Cryptic Cysteines.

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins

Alterations at the Cross-Bridge Level Are Associated with a Paradoxical Gain of Muscle Function In Vivo in a Mouse Model of Nemaline Myopathy

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins.

Alterations at the Cross-Bridge Level Are Associated with a Paradoxical Gain of Muscle Function In Vivo in a Mouse Model of Nemaline Myopathy.

E258K HCM-causing mutation in cardiac MyBP-C reduces contractile force and accelerates twitch kinetics by disrupting the cMyBP-C and myosin S2 interaction.

Force measurement during contraction to assess muscle function in zebrafish larvae.

Calcium sensitivity and myofilament lattice structure in titin N2B KO mice.

Troponin activator augments muscle force in nemaline myopathy patients with nebulin mutations.

Calcium sensitivity and myofilament lattice structure in titin N2B KO mice.

A gain-of-function mutation in the M-domain of cardiac myosin-binding protein-C increases binding to actin.

Effects of alterations in sarcomere structure and prestretch timing on cardiac muscle mechanics.

Factors underlying the early limb muscle weakness in acute quadriplegic myopathy using an experimental ICU porcine model.

Calcium sensitivity and the Frank-Starling mechanism of the heart are increased in titin N2B region-deficient mice.

ltered contractility of skeletal muscle in mice deficient in titin’s M-band region.

Cross-bridge interaction kinetics in rat myocardium are accelerated by strong binding of myosin to the thin filament.

Altered contractility of skeletal muscle in mice deficient in titin’s M-band region.

The increase in non-cross-bridge forces after stretch of activated striated muscle is related to titin isoforms.

Computing Average Passive Forces in Sarcomeres in Length-Ramp Simulations .

Effect of levosimendan on the contractility of muscle fibers from nemaline myopathy patients with mutations in the nebulin gene.

Pompe disease results in a Golgi-based glycosylation deficit in human induced pluripotent stem cell-derived cardiomyocytes.

Alterations at the Cross-Bridge Level Are Associated with a Paradoxical Gain of Muscle Function In Vivo in a Mouse Model of Nemaline Myopathy.

Muscle histopathology in nebulin-related nemaline myopathy: ultrastrastructural findings correlated to disease severity and genotype.

Large-Scale Modulation of Titin Elasticity by S-Glutathionylation of Cryptic Cysteines.

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins

Alterations at the Cross-Bridge Level Are Associated with a Paradoxical Gain of Muscle Function In Vivo in a Mouse Model of Nemaline Myopathy

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins.

Alterations at the Cross-Bridge Level Are Associated with a Paradoxical Gain of Muscle Function In Vivo in a Mouse Model of Nemaline Myopathy.

E258K HCM-causing mutation in cardiac MyBP-C reduces contractile force and accelerates twitch kinetics by disrupting the cMyBP-C and myosin S2 interaction.

Force measurement during contraction to assess muscle function in zebrafish larvae.

Calcium sensitivity and myofilament lattice structure in titin N2B KO mice.

Troponin activator augments muscle force in nemaline myopathy patients with nebulin mutations.

Calcium sensitivity and myofilament lattice structure in titin N2B KO mice.

A gain-of-function mutation in the M-domain of cardiac myosin-binding protein-C increases binding to actin.

Effects of alterations in sarcomere structure and prestretch timing on cardiac muscle mechanics.

Factors underlying the early limb muscle weakness in acute quadriplegic myopathy using an experimental ICU porcine model.

Calcium sensitivity and the Frank-Starling mechanism of the heart are increased in titin N2B region-deficient mice.

ltered contractility of skeletal muscle in mice deficient in titin’s M-band region.

Cross-bridge interaction kinetics in rat myocardium are accelerated by strong binding of myosin to the thin filament.

Altered contractility of skeletal muscle in mice deficient in titin’s M-band region.

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