Force loss in skeletal muscle exposed to eccentric contraction is often attributed to injury. We
show that EDL muscles from dystrophin-deficient mdx mice recover 65% of lost force within …

Increased production of reactive oxygen/nitrogen species (ROS) and impaired cellular Ca2+
handling are implicated in the prolonged low‐frequency force depression (PLFFD) observed …

Experimental models of cardiac disease play a key role in understanding the
pathophysiology of the disease and developing new therapies. The features of the …

Aims The microtubule (MT) network plays a major role in the transport of the cardiac sodium
channel Nav1. 5 to the membrane, where the latter associates with interacting proteins such …

In heart failure, an increased abundance of post-translationally detyrosinated microtubules
stiffens the cardiomyocyte and impedes its contractile function. Detyrosination promotes …

In non-excitable cells stromal interaction molecule 1 (STIM1) is a key element in the
generation of Ca2+ signals that lead to gene expression, migration and cell proliferation. A …

Tubulin posttranslational modifications (PTMs) add “tubulin code” to generate functional
diversities of microtubules. Several types of tubulin PTMs accumulate on axonemes and …

The highly ordered cortical microtubule lattice of skeletal muscle is disorganized in
dystrophin-deficient mdx mice. Implicated mechanisms include loss of dystrophin binding …

The giant muscle protein titin is a major contributor to passive force; however, its role in
active force generation is unresolved. Here, we use a novel titin-cleavage (TC) mouse …

Nemaline myopathy (NM) is a skeletal muscle disorder caused by mutations in genes that
are generally involved in muscle contraction, in particular those related to the structure …