Kay Davies, CBE, DBE, FMedSci, FRS | DuchenneXchange

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Researchers

Kay Davies, CBE, DBE, FMedSci, FRS

Researcher
Director, MRC Functional Genomics Unit
Department of Physiology, Anatomy and Genetics
Medical Science Division
University of Oxford
Sherrington Building, Parks Road
Oxford, United Kingdom

Dr. Kay Davies is elected Dr. Lee’s Professor of Anatomy at the University of Oxford. She worked as the Head of Department from 2008 to 2011. She is also the co-founder and presently the director of MRC Functional Genomics Unit. This unit aims at exploiting genome information for the analysis of the function of genes in the nervous system.  Dr. Kay Davies is the co-founder and co-director of the Oxford Centre of Gene Function with Professors Ashcroft (Physiology) and Donnelly (Statistics), which brings together genetics, physiology, and bioinformatics in a new multidisciplinary building. She is a founding fellow of the Academy of Medical Sciences and was elected as a Fellow of the Royal Society in 2003.

Dr. Davies research interests include the molecular analysis of human genetic disease, primarily focused on the genetic basis of neuromuscular and neurological disorders. She worked on muscular dystrophy for more than 20 years and many of her research groups are dedicated to finding effective treatments for Duchenne muscular dystrophy (DMD) and spinal muscular atrophy. She has an active interest in the ethical implications of her research and in the public understanding of science.

 

Representative Publications:

Safety, Tolerability, and Pharmacokinetics of SMT C1100, a 2-Arylbenzoxazole Utrophin Modulator, following Single- and Multiple-Dose Administration to Pediatric Patients with Duchenne Muscular Dystrophy

Pharmacological advances for treatment in Duchenne muscular dystrophy

Engineering multiple U7snRNA constructs to induce single and multiexon-skipping for Duchenne Muscular Dystrophy

Modified patient stem cells as prelude to autologous treatment of muscular dystrophy

Alternative utrophin mRNAs contribute to phenotypic differences between dystrophin-deficient mice and Duchenne muscular dystrophy

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