K
Kay E. Davies
Researcher at University of Oxford
Publications - 580
Citations - 40236
Kay E. Davies is an academic researcher from University of Oxford. The author has contributed to research in topics: Duchenne muscular dystrophy & Dystrophin. The author has an hindex of 100, co-authored 573 publications receiving 38462 citations. Previous affiliations of Kay E. Davies include Case Western Reserve University & Technische Universität München.
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Journal ArticleDOI
Candidate screening of the TRPC3 gene in cerebellar ataxia.
Esther B. E. Becker,Brent L. Fogel,Sanjeev Rajakulendran,Anna Dulneva,Michael G. Hanna,Susan Perlman,Daniel H. Geschwind,Kay E. Davies +7 more
TL;DR: It is suggested that mutations in TRPC3 do not significantly contribute to the cause of late-onset and episodic human cerebellar ataxias.
Journal ArticleDOI
Embryonic myosin is a regeneration marker to monitor utrophin-based therapies for DMD.
Simon Guiraud,Benjamin Edwards,Sarah E. Squire,Lee Moir,Adam Berg,Arran Babbs,Nesrine Ramadan,Matthew J.A. Wood,Kay E. Davies +8 more
TL;DR: It is demonstrated that MyHC-emb is a robust marker of regeneration at different ages and in different skeletal muscles and provides translational support for the use of developmental myosin as a disease biomarker in DMD clinical trials.
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Challenges to oligonucleotides-based therapeutics for Duchenne muscular dystrophy
Aurélie Goyenvalle,Kay E. Davies +1 more
TL;DR: In this review, the recent developments and clinical trials using antisense oligonucleotides for Duchenne muscular dystrophy are discussed, with emphasis on the challenges ahead for this type of therapy, especially with regards to delivery and regulatory issues.
Journal ArticleDOI
Chemical Proteomics and Phenotypic Profiling Identifies the Aryl Hydrocarbon Receptor as a Molecular Target of the Utrophin Modulator Ezutromid
Wilkinson Ivl.,Kelly J. Perkins,H Dugdale,Lee Moir,A Vuorinen,Maria Chatzopoulou,Sarah E. Squire,S Monecke,A Lomow,M Geese,Philip D. Charles,P Burch,Jonathon M. Tinsley,Graham Michael Wynne,Stephen G. Davies,F. Wilson,Fraydoon Rastinejad,Shabaz Mohammed,Kay E. Davies,Angela J. Russell +19 more
TL;DR: It is shown that the aryl hydrocarbon receptor (AhR) is a target of ezutromid and other reported AhR antagonists also upregulate utrophin, showing that this pathway, which is currently being explored in other clinical applications including oncology and rheumatoid arthritis, could also be exploited in future DMD therapies.