J
John C. W. Hildyard
Researcher at Royal Veterinary College
Publications - 24
Citations - 900
John C. W. Hildyard is an academic researcher from Royal Veterinary College. The author has contributed to research in topics: Duchenne muscular dystrophy & Dystrophin. The author has an hindex of 9, co-authored 20 publications receiving 655 citations. Previous affiliations of John C. W. Hildyard include University of Warwick & University of Bristol.
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Journal ArticleDOI
Gene editing restores dystrophin expression in a canine model of Duchenne muscular dystrophy
Leonela Amoasii,John C. W. Hildyard,Hui Li,Efrain Sanchez-Ortiz,Alex A. Mireault,Daniel Caballero,R. Harron,Thaleia-Rengina Stathopoulou,Claire Massey,John M. Shelton,Rhonda Bassel-Duby,Richard J. Piercy,Eric N. Olson +12 more
TL;DR: Large-animal data support the concept that gene editing approaches may prove clinically useful for the treatment of DMD, and successful CRISPR correction of a dystrophin mutation in dogs increases dystrophicin protein expression in skeletal and heart muscle.
Journal ArticleDOI
Identification and characterisation of a new class of highly specific and potent inhibitors of the mitochondrial pyruvate carrier.
TL;DR: Two novel thiazolidine compounds, GW604714X and GW450863X, were found to be potent inhibitors of mitochondrial respiration supported by pyruvate but not other substrates, suggesting that the covalent modification is reversible.
Journal ArticleDOI
How much dystrophin is enough: the physiological consequences of different levels of dystrophin in the mdx mouse
Caroline Godfrey,S Muses,Graham McClorey,K E Wells,Thibault Coursindel,R L Terry,Corinne A. Betts,Suzan M. Hammond,Liz O'Donovan,John C. W. Hildyard,S El Andaloussi,M J Gait,Matthew J.A. Wood,Dominic J. Wells +13 more
TL;DR: The dystrophin restoration levels required to slow down or prevent disease progression and improve overall muscle function once a dystrophic environment has been established in the mdx mouse model are defined.
Journal ArticleDOI
Identification of the mitochondrial pyruvate carrier in Saccharomyces cerevisiae.
TL;DR: This work has identified the yeast mitochondrial pyruvate carrier by measuring inhibitor-sensitive pyruVate uptake into mitochondria from 18 different Saccharomyces cerevisiae mutants, each lacking an unattributed member of the mitochondrial carrier family (MCF).
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Identification and validation of quantitative PCR reference genes suitable for normalizing expression in normal and dystrophic cell culture models of myogenesis
TL;DR: The data show that Csnk2a2 and Ap3d1 are suitable for normalizing gene expression during differentiation in both healthy and dystrophic cell-culture models, and that the commonly-used reference standards 18S, ActB and GAPDH are exceptionally poor candidates.