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Biography and Research Information
OverviewAI-generated summary
Michele Yang's research focuses on the study of genetic and neuromuscular disorders, particularly Duchenne muscular dystrophy (DMD). Her work has investigated the efficacy and safety of therapeutic agents, such as vamorolone, over extended periods in pediatric populations with DMD. Yang has also explored the genetic underpinnings of neurodevelopmental disorders, including identifying loss-of-function mutations in the GEMIN5 gene. Her research extends to the development and validation of assessment tools, such as hyperphagia questionnaires for patients with Bardet-Biedl syndrome.
Her recent publications also address clinical considerations in managing rare genetic conditions, including gene therapy delivery for DMD and treatment outcomes for spinal muscular atrophy. Yang has contributed to understanding biomarker identification in DMD patient cohorts and has examined healthcare access during the COVID-19 pandemic, specifically the utilization of telemedicine in neurology.
Yang leads a research group and has a h-index of 26 with over 2,700 citations across 74 publications. She collaborates with other researchers at the University of Arkansas for Medical Sciences, including Aravindhan Veerapandiyan. Her recent activity indicates ongoing contributions to the field.
Metrics
- h-index: 26
- Publications: 74
- Citations: 2,732
Selected Publications
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Consensus recommendations and considerations for the delivery and monitoring of gene therapy in patients with Duchenne muscular dystrophy (2025)
Collaboration Network
Top Collaborators
- Efficacy and Safety of Vamorolone Over 48 Weeks in Boys With Duchenne Muscular Dystrophy
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- Circulating protein biomarkers identified in two independent clinical trial cohorts of glucocorticoid-naive Duchenne muscular dystrophy patients.
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- 595P ACTA1-related cardiomyopathy: emerging genotypic and phenotypic patterns among patients with ACTA1-related myopathy with cardiac involvement
- Efficacy and Safety of Vamorolone Over 48 Weeks in Boys With Duchenne Muscular Dystrophy
- Loss of function mutations in GEMIN5 cause a neurodevelopmental disorder
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin
- P236 Rod-less dystrophin may exert a dominant negative effect by interfering with utrophin's function
- Efficacy and Safety of Vamorolone Over 48 Weeks in Boys With Duchenne Muscular Dystrophy
- Circulating protein biomarkers identified in two independent clinical trial cohorts of glucocorticoid-naive Duchenne muscular dystrophy patients.
- Efficacy and Safety of Vamorolone Over 48 Weeks in Boys With Duchenne Muscular Dystrophy
- Circulating protein biomarkers identified in two independent clinical trial cohorts of glucocorticoid-naive Duchenne muscular dystrophy patients.
- Efficacy and Safety of Vamorolone Over 48 Weeks in Boys With Duchenne Muscular Dystrophy
- Circulating protein biomarkers identified in two independent clinical trial cohorts of glucocorticoid-naive Duchenne muscular dystrophy patients.
- Efficacy and Safety of Vamorolone Over 48 Weeks in Boys With Duchenne Muscular Dystrophy
- Circulating protein biomarkers identified in two independent clinical trial cohorts of glucocorticoid-naive Duchenne muscular dystrophy patients.
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