Radically truncated MeCP2 rescues Rett syndrome-like neurological defects

Rebekah Tillotson, Jim Selfridge, Martha V. Koerner, Kamal K. E. Gadalla, Jacky Guy, Dina De Sousa, Ralph D. Hector, Stuart R. Cobb and Adrian Bird ()
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Rebekah Tillotson: The Wellcome Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King’s Buildings, Max Born Crescent
Jim Selfridge: The Wellcome Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King’s Buildings, Max Born Crescent
Martha V. Koerner: The Wellcome Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King’s Buildings, Max Born Crescent
Kamal K. E. Gadalla: Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow
Jacky Guy: The Wellcome Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King’s Buildings, Max Born Crescent
Dina De Sousa: The Wellcome Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King’s Buildings, Max Born Crescent
Ralph D. Hector: Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow
Stuart R. Cobb: Institute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow
Adrian Bird: The Wellcome Centre for Cell Biology, University of Edinburgh, Michael Swann Building, King’s Buildings, Max Born Crescent

Nature, 2017, vol. 550, issue 7676, 398-401

Abstract: Analysis of the minimal functional unit for MeCP2 protein shows that its function is to recruit the NCoR/SMRT co-repressor complex to methylated sites on chromatin, which may have use in designing strategies for gene therapy of Rett syndrome.

Date: 2017
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DOI: 10.1038/nature24058

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