David L. Mack

This paper introduces GERALT, a genetic circuit that enables TGFβ-independent hiPSC renewal and inducible lineage programming, improving differentiation efficiency and reducing medium complexity.

This study uses patient-derived iPSCs to create 2D and 3D muscle models that replicate RYR1 myopathy phenotypes and test therapeutic efficacy.

This paper demonstrates that AI-designed receptor modulators can drive efficient human fibroblast-to-muscle transdifferentiation by rewiring extracellular signaling.

The paper shows that voluntary running maintains gene expression corrections from AAV gene therapy in mdx mice, indicating physical exercise does not negatively affect therapy outcomes.

This study uses engineered human muscle tissues to evaluate AAV capsid efficiency, finding that more mature tissues show improved transduction by AAV9 and MyoAAV variants.

The paper identifies a dynamic gene regulatory network in Duchenne muscular dystrophy that controls cell fate decisions and shows how disease mutations disrupt this network.

This paper designs a synthetic ligand, H2F, that induces HER2-FGFR proximity to reprogram fibroblasts into myogenic cells and promote myogenic regeneration.

This study shows that dystrophin deficiency disrupts cell junction formation during embryonic myogenesis in human pluripotent stem cells.

This study shows that YAP overactivation in HCM mutant cardiomyocytes drives hypertrophy via CCN2 secretion and TGFβ uptake.

This paper introduces a new fluorescent sensor, oROS-HT, for real-time H2O2 monitoring with subcellular resolution and multi-parametric imaging capabilities.

This paper develops a fast, sensitive genetically encoded H2O2 sensor (oROS-G) and demonstrates its use in monitoring H2O2 dynamics in various cell types and models.

This study investigates the effects of the MYH7 G256E mutation on myosin function across multiple scales, finding increased hypercontractility and mitochondrial respiration.

This study shows that interferon-gamma exposure causes TDP-43 mislocalization and ALS-like pathology in human motor neurons.