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Sabine M. Klauck

Researcher at German Cancer Research Center

Publications -  85
Citations -  18648

Sabine M. Klauck is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Autism & Gene. The author has an hindex of 37, co-authored 80 publications receiving 16756 citations. Previous affiliations of Sabine M. Klauck include University of Pennsylvania.

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Synaptic, transcriptional and chromatin genes disrupted in autism

Silvia De Rubeis, +99 more
- 13 Nov 2014 - 
TL;DR: Using exome sequencing, it is shown that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate of < 0.05, plus a set of 107 genes strongly enriched for those likely to affect risk (FDR < 0.30).
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Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs

S. Hong Lee, +405 more
- 01 Sep 2013 - 
TL;DR: Empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.
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Functional impact of global rare copy number variation in autism spectrum disorders

Dalila Pinto, +181 more
- 15 Jul 2010 - 
TL;DR: The genome-wide characteristics of rare (<1% frequency) copy number variation in ASD are analysed using dense genotyping arrays to reveal many new genetic and functional targets in ASD that may lead to final connected pathways.
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Analysis of shared heritability in common disorders of the brain

Verneri Anttila, +720 more
- 22 Jun 2018 - 
TL;DR: It is demonstrated that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine, and it is shown that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures.
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Mapping autism risk loci using genetic linkage and chromosomal rearrangements

Peter Szatmari, +139 more
- 01 Mar 2007 - 
TL;DR: Linkage and copy number variation analyses implicate chromosome 11p12–p13 and neurexins, respectively, among other candidate loci, highlighting glutamate-related genes as promising candidates for contributing to ASDs.