Matthew S. Alexander

This paper deletes Dock7 exons 3-4 in mice, resulting in reduced trabecular bone volume and altered osteoblast function.

This study investigates the role of DOCK7 in skeletal muscle and motor neurons, showing its regulation of WNT signaling and AChR clustering in both normal and DMD muscle.

The paper identifies a BMP4-induced molecular signature in late-stage DMD skeletal muscle by comparing transcriptomes of DMD patients and BMP4-stimulated cells.

This paper describes the generation of zebrafish models carrying specific human disease variants using CRISPR/Cas9 and ssODNs, with methods to evaluate HDR efficiency and genotype F1 animals.

This study investigates the effects of conditional dystrophin ablation in skeletal muscle and brain, revealing functional deficits and pathway dysregulation in both tissues.

This study shows that DOCK3 is essential for skeletal muscle regeneration and glucose metabolism, with its loss causing metabolic dysfunction and impaired muscle repair.

The paper shows miR-486 is reduced in DMD muscles and its loss causes muscle and cardiac defects, identifying it as a driver of disease and a potential biomarker.

This study investigates the role of DOCK3 in skeletal muscle and Duchenne muscular dystrophy, finding that reducing DOCK3 improves dystrophic muscle histology while complete loss worsens muscle function.