J
Jacky Guy
Researcher at University of Edinburgh
Publications - 32
Citations - 6281
Jacky Guy is an academic researcher from University of Edinburgh. The author has contributed to research in topics: MECP2 & Rett syndrome. The author has an hindex of 21, co-authored 31 publications receiving 5776 citations. Previous affiliations of Jacky Guy include Erasmus University Rotterdam.
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Journal ArticleDOI
A mouse Mecp2-null mutation causes neurological symptoms that mimic rett syndrome
TL;DR: The overlapping delay before symptom onset in humans and mice raises the possibility that stability of brain function, not brain development per se, is compromised by the absence of MeCP2, and generates mice lacking Mecp2 using Cre-loxP technology.
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Reversal of Neurological Defects in a Mouse Model of Rett Syndrome
TL;DR: Using a mouse model, robust phenotypic reversal is demonstrated, as activation of MeCP2 expression leads to striking loss of advanced neurological symptoms in both immature and mature adult animals.
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CpG islands influence chromatin structure via the CpG-binding protein Cfp1
John P. Thomson,Peter J Skene,Jim Selfridge,Thomas Clouaire,Jacky Guy,Shaun Webb,Alastair R.W. Kerr,Aimee M. Deaton,Robert Andrews,Keith D. James,Daniel J. Turner,Robert S. Illingworth,Adrian Bird +12 more
TL;DR: The data indicate that a primary function of non-methylated CGIs is to genetically influence the local chromatin modification state by interaction with Cfp1 and perhaps other CpG-binding proteins.
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The Role of MeCP2 in the Brain
TL;DR: Two alternative views of MeCP2 in the brain are considered: as a regulator of brain development or as a factor that helps maintain neuronal/glial function.
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Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor
Matthew J. Lyst,Robert Ekiert,Daniel H. Ebert,Cara Merusi,Jakub Stanislaw Nowak,Jim Selfridge,Jacky Guy,Nathaniel R. Kastan,Nathaniel D. Robinson,Flavia de Lima Alves,Juri Rappsilber,Michael E. Greenberg,Adrian Bird +12 more
TL;DR: These data are compatible with the hypothesis that brain dysfunction in RTT is caused by a loss of the MeCP2 'bridge' between the NCoR/SMRT co-repressors and chromatin.