Cardiac-specific overexpression of a recently discovered micropeptide, DWORF, enhances calcium cycling and contractility in the heart and rescues the heart failure phenotype of a genetic mouse model of dilated cardiomyopathy.
Maintenance of peripheral myonuclei patterning in skeletal myofibers is dependent on the regulation of microtubules dynamic and nuclei motion and is essential for proper neuromuscular junction integrity and mitochondria homeostasis.
Single and double-knockout mouse models for proteins associated with nodes of Ranvier reveal that a paranodal, spectrin-based lateral diffusion barrier is sufficient to cluster Na+ channels at nodes of Ranvier.
The amount of secreted Pgk1 is sharply decreased in Rtn4al/NogoA-overexpressed muscle cells, leading to various manifestations of neurodegenerative disease, including denervated neuromuscular junction and failed neurite outgrowth of motoneurons.
Knockout of the methyltransferase ICMT prevents progerin methylation and improves survival in mice with Hutchinson-Gilford progeria syndrome (HGPS) and an ICMT inhibitor delays senescence and stimulates proliferation of HGPS cells.
Activity-dependent genetic labeling during behavioral learning shows Fragile-X syndrome model mice exhibit impaired hippocampal engram reactivation, and that enriched environment experience improves fear memory retrieval by enhancing engram reactivation efficacy.
Comparative -omic analyses of five knockout mouse strains with disrupted mitochondrial DNA expression at different levels provide a high quality resource of altered gene expression patterns that reveal several common secondary patophysiological changes of mitochondrial dysfunction.