Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Project (R01)
Project #
2R01MH052708-02
Application #
2034158
Study Section
Epidemiology and Genetics Review Committee (EPI)
Project Start
1995-07-01
Project End
2000-06-30
Budget Start
1996-09-30
Budget End
1997-06-30
Support Year
2
Fiscal Year
1996
Total Cost
Indirect Cost
Name
Stanford University
Department
Genetics
Type
Schools of Medicine
DUNS #
800771545
City
Stanford
State
CA
Country
United States
Zip Code
94305
Correia, Catarina; Oliveira, Guiomar; Vicente, Astrid M (2014) Protein interaction networks reveal novel autism risk genes within GWAS statistical noise. PLoS One 9:e112399
Gaugler, Trent; Klei, Lambertus; Sanders, Stephan J et al. (2014) Most genetic risk for autism resides with common variation. Nat Genet 46:881-5
Tsang, Kathryn M; Croen, Lisa A; Torres, Anthony R et al. (2013) A genome-wide survey of transgenerational genetic effects in autism. PLoS One 8:e76978
Sampath, Srirangan; Bhat, Shambu; Gupta, Simone et al. (2013) Defining the contribution of CNTNAP2 to autism susceptibility. PLoS One 8:e77906
Anney, Richard; Klei, Lambertus; Pinto, Dalila et al. (2012) Individual common variants exert weak effects on the risk for autism spectrum disorders. Hum Mol Genet 21:4781-92
Casey, Jillian P; Magalhaes, Tiago; Conroy, Judith M et al. (2012) A novel approach of homozygous haplotype sharing identifies candidate genes in autism spectrum disorder. Hum Genet 131:565-79
Anney, Richard J L; Kenny, Elaine M; O'Dushlaine, Colm et al. (2011) Gene-ontology enrichment analysis in two independent family-based samples highlights biologically plausible processes for autism spectrum disorders. Eur J Hum Genet 19:1082-9
Pinto, Dalila; Pagnamenta, Alistair T; Klei, Lambertus et al. (2010) Functional impact of global rare copy number variation in autism spectrum disorders. Nature 466:368-72
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Fradin, Delphine; Cheslack-Postava, Keely; Ladd-Acosta, Christine et al. (2010) Parent-of-origin effects in autism identified through genome-wide linkage analysis of 16,000 SNPs. PLoS One 5:

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