J
Jim Selfridge
Researcher at University of Edinburgh
Publications - 43
Citations - 5628
Jim Selfridge 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 26, co-authored 42 publications receiving 5196 citations.
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Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
Embryonic lethal phenotype reveals a function of TDG in maintaining epigenetic stability
Daniel Cortázar,Christophe Kunz,Jim Selfridge,Teresa Lettieri,Teresa Lettieri,Yusuke Saito,Eilidh MacDougall,Annika Wirz,David Schuermann,Angelika L. Jacobs,Fredy Siegrist,Roland Steinacher,Roland Steinacher,Josef Jiricny,Adrian Bird,Primo Schär +15 more
TL;DR: It is shown that TDG contributes to the maintenance of active and bivalent chromatin throughout cell differentiation, facilitating a proper assembly of chromatin-modifying complexes and initiating base excision repair to counter aberrant de novo methylation, and has evolved to provide epigenetic stability in lineage committed cells.
Journal ArticleDOI
Mice with DNA repair gene ( ERCC-1 ) deficiency have elevated levels of p53, liver nuclear abnormalities and die before weaning
TL;DR: Elevated p53 levels were detected in liver, brain and kidney, supporting the hypothesised role for p53 as a monitor of DNA damage in mice with defective DNA repair.