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3. The administration of antisense oligonucleotide golodirsen reduces pathological regeneration in patients with Duchenne muscular dystrophy

8. A new patient‐derived iPSC model for dystroglycanopathies validates a compound that increases glycosylation of α‐dystroglycan

10. A Proof of Principle Proteomic Study Detects Dystrophin in Human Plasma : Implications in DMD Diagnosis and Clinical Monitoring

11. A Proof of Principle Proteomic Study Detects Dystrophin in Human Plasma: Implications in DMD Diagnosis and Clinical Monitoring

13. Mutations in GDP-Mannose Pyrophosphorylase B Cause Congenital and Limb-Girdle Muscular Dystrophies Associated with Hypoglycosylation of α-Dystroglycan

14. Mutations in B3GALNT2 Cause Congenital Muscular Dystrophy and Hypoglycosylation of α-Dystroglycan

16. Exon skipping and dystrophin restoration in patients with Duchenne muscular dystrophy after systemic phosphorodiamidate morpholino oligomer treatment: an open-label, phase 2, dose-escalation study

19. Investigating the role of dystrophin isoform deficiency in motor function in Duchenne muscular dystrophy

20. TRAPPC11 ‐related muscular dystrophy with hypoglycosylation of alpha‐dystroglycan in skeletal muscle and brain

21. Urine-Derived Stem Cells Express 571 Neuromuscular Disorders Causing Genes, Making Them a Potential in vitro Model for Rare Genetic Diseases

22. High-Throughput Digital Image Analysis Reveals Distinct Patterns of Dystrophin Expression in Dystrophinopathy Patients

24. Duchenne muscular dystrophy patients lacking the dystrophin isoforms Dp140 and Dp71 and mouse models lacking Dp140 have a more severe motor phenotype

25. TRAPPC11-related muscular dystrophy with hypoglycosylation of alpha-dystroglycan in skeletal muscle and brain

26. Urine-Derived Stem Cells Express 571 Neuromuscular Disorders Causing Genes, Making Them a Potential in vitro Model for Rare Genetic Diseases

29. ISPD gene mutations are a common cause of congenital and limb-girdle muscular dystrophies

30. Defective glycosylation in muscular dystrophy. (Rapid Review)

31. Mutations in the fukutin-related protein gene (FKRP) cause a form of congenital muscular dystrophy with secondary laminin [alpha]2 deficiency and abnormal glycosylation of [alpha]-Dystroglycan

32. Dystrophin quantification and clinical correlations in Becker muscular dystrophy: implications for clinical trials

34. TRAPPC11-related muscular dystrophy with hypoglycosylation of alpha-dystroglycan in skeletal muscle and brain.

35. POMK regulates dystroglycan function via LARGE1-mediated elongation of matriglycan

36. Author response: POMK regulates dystroglycan function via LARGE1-mediated elongation of matriglycan

37. POMK regulates dystroglycan function via LARGE-mediated elongation of matriglycan

38. A Comparative Study of α-Dystroglycan Glycosylation in Dystroglycanopathies Suggests that the Hypoglycosylation of α-Dystroglycan Does Not Consistently Correlate with Clinical Severity

40. TRAPPC11‐related muscular dystrophy with hypoglycosylation of alpha‐dystroglycan in skeletal muscle and brain.

43. Refining genotype–phenotype correlations in muscular dystrophies with defective glycosylation of dystroglycan

48. Mutations in the fukutin-related protein gene (FKRP) identify limb girdle muscular dystrophy 2I as a milder allelic variant of congenital muscular dystrophy MDC1C

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