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Genetic interactions drive heterogeneity in causal variant effect sizes for gene expression and complex traits
Affiliation:1. Genetics, Stanford University School of Medicine, Stanford, CA, USA;2. VA Palo Alto Health Care System, Palo Alto, CA, USA;3. Computational Medicine, University of California, Los Angeles, Los Angeles, CA, USA;4. Human Genetics, University of California, Los Angeles, Los Angeles, CA, USA;5. Stanford University School of Medicine, Stanford, CA, USA;6. The Robert Larner, M.D. College of Medicine at The University of Vermont, Burlington, VT, USA;7. Institute for Translational Genomics and Population Sciences, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA;8. Duke University School of Medicine, Durham, NC, USA;9. Biostatistics, University of Washington, Seattle, WA, USA;10. Broad Institute of MIT and Harvard, Cambridge, MA, USA;11. Genome Sciences, University of Washington, Seattle, WA, USA;12. Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA;13. Biology, Stanford University, Stanford, CA, USA
Abstract:
Keywords:statistical genetics  complex traits  genome-wide association  genetic correlation  population genetics
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