Markus A. Rüegg

This study shows that laminin-α2 is essential for maintaining the myotendinous junction structure, and mechanical unloading affects its integrity in a mouse model of LAMA2-related muscular dystrophy.

This study identifies c-MAF as a mediator of motoneuron activity in maintaining fast-glycolytic muscle fibers and neuromuscular junctions through chromatin accessibility changes and gene regulation.

This paper describes a dual AAV gene therapy approach using linker proteins to restore basement membrane function in LAMA2 MD, showing significant improvements in muscle and nerve defects.

This study shows that laminin-α2 secreted by muscle stem cells is critical for their expansion and regeneration, and its loss leads to muscle stem cell dysfunction in LAMA2-related muscular dystrophy.

The paper shows mini-agrin prevents calcium leakage and restores the dystrophin complex in dystrophic muscle cells by stabilizing CaV1.1 and reconstituting dystrophin complex components.

This study shows that transplanting iPSC-derived neural progenitor cells improves long-term recovery after stroke in mice by promoting tissue repair and reducing neurological deficits.

This study shows that muscle fiber Myc is not required for muscle growth but its overexpression disrupts muscle structure and function.

The paper uses single-nuclei RNA-sequencing to identify NMJ-specific transcripts and shows that Etv4 and Pdzrn4 contribute to NMJ stability through gene regulation and protein interactions.

This study develops a method to efficiently induce somatic gene deletions in adult mouse skeletal muscle fibers using AAV-CRISPR/Cas9, replicating knockout phenotypes without generating knockout mice.

This study shows that expressing two linker proteins in mouse models of LAMA2-related muscular dystrophy improves muscle function and prevents hindlimb paralysis.

This study shows that mTORC1 inhibition in adult mice does not cause muscle atrophy or functional decline, despite metabolic and morphological changes.