Research article
Genomic and epigenetic evidence for oxytocin receptor deficiency in autism
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* Corresponding author: Simon G Gregory simon.gregory@duke.edu
- † Equal contributors
1 Duke Center for Human Genetics, DUMC, Durham, NC, USA
2 Laboratory of Molecular Psychiatry & Neurogenetics, University Campus Bio-Medico, Rome, Italy
3 IRCCS 'Fondazione Santa Lucia', Rome, Italy
4 Department of Neuropsychiatry, SOM-USC, Columbia, SC, USA
5 Wellcome Trust Sanger Institute, Hinxton, UK
6 Duke Department of Medicine, DUMC, Durham, NC, USA
7 Departments of Obstetrics and Gynecology, and Pathology, Duke University, Durham, NC, USA
8 John P Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, FL, USA
BMC Medicine 2009, 7:62 doi:10.1186/1741-7015-7-62
Published: 22 October 2009Additional files
Additional file 1:
Cloned bisulfite sequencing results for each peripheral blood mononuclear cell (PBMC) sample.
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Additional file 2:
Primer pairs used for this study.
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Additional file 3:
Genomic duplication and deletion events within 54 control and 119 autistic individuals identified by whole genome tilepath array comparative genomic hybridization (CGH).
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Additional file 4:
OXTR promoter CpG methylation status in peripheral blood mononuclear cells (PBMCs) of 10 autistic females and 10 age-matched controls.
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Additional file 5:
OXTR promoter CpG methylation status in the cortex of eight autism cases and controls matched for age and sex.
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