Science Advances

Supplementary Materials

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  • Fig. S1. Muscle-specific transgenic overexpression of ML1.
  • Fig. S2. Muscle-specific transgenic overexpression of ML1 reduces GAS, DIA, and cardiac pathologies in mdx mice.
  • Fig. S3. Pharmacokinetics and toxicity of ML-SA5.
  • Fig. S4. ML1 agonist injection (intraperitoneal) ameliorates GAS and DIA pathologies in mdx mice.
  • Fig. S5. Activation of ML1 corrects lysosomal insufficiency and improves sarcolemmal repair in mdx mice.
  • Fig. S6. ML1 agonist activates TFEB/TFE3 and lysosomal biogenesis in DMD myoblasts.
  • Fig. S7. Sarcolemmal Ca2+ entry is not required for ML-SA–induced TFEB nuclear translocation.
  • Fig. S8. ML1 agonist prevents cell death in DMD myoblasts via TFEB.
  • Fig. S9. Lysosomal exocytosis is required for ML-SA5–induced sarcolemma repair and cell survival.
  • Fig. S10. Requirement of continuous agonist administration in achieving muscle protective effects.

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