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Times Cited
Times Co-cited
Similarity
Synaptic, transcriptional and chromatin genes disrupted in autism.
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The contribution of de novo coding mutations to autism spectrum disorder.
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Insights into Autism Spectrum Disorder Genomic Architecture and Biology from 71 Risk Loci.
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De novo mutations revealed by whole-exome sequencing are strongly associated with autism.
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Most genetic risk for autism resides with common variation.
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Transcriptomic analysis of autistic brain reveals convergent molecular pathology.
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Multiple recurrent de novo CNVs, including duplications of the 7q11.23 Williams syndrome region, are strongly associated with autism.
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Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations.
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Identification of common genetic risk variants for autism spectrum disorder.
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The familial risk of autism.
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Disruptive CHD8 mutations define a subtype of autism early in development.
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Coexpression networks implicate human midfetal deep cortical projection neurons in the pathogenesis of autism.
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Common genetic variants, acting additively, are a major source of risk for autism.
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Strong association of de novo copy number mutations with autism.
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Big data approaches to decomposing heterogeneity across the autism spectrum.
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Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.