ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014
Fine mapping on chromosome 13q32-34 and brain expression analysis implicates MYO16 in schizophrenia.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 42 citations in OpenAlex.
- Genetic architecture of the structural connectome.Nature communications · 2024Article
- Admixture mapping implicates 13q33.3 as ancestry-of-origin locus for Alzheimer disease in Hispanic and Latino populations.HGG advances · 2023Article
- Positive Selection and Enhancer Evolution Shaped Lifespan and Body Mass in Great Apes.Molecular biology and evolution · 2022Article
- The C-terminal tail extension of myosin 16 acts as a molten globule, including intrinsically disordered regions, and interacts with the N-terminal ankyrin.The Journal of biological chemistry · 2021Article
- Multi-trait GWAS using imputed high-density genotypes from whole-genome sequencing identifies genes associated with body traits in Nile tilapia.BMC genomics · 2021Article
- Myosin XVI in the Nervous System.Cells · 2020Review
- Altered gene expression in antipsychotic-induced weight gain.NPJ schizophrenia · 2019Article
- Myosin XVI Regulates Actin Cytoskeleton Dynamics in Dendritic Spines of Purkinje Cells and Affects Presynaptic Organization.Frontiers in cellular neuroscience · 2019Article
- PPARgamma agonists rescue increased phosphorylation of FGF14 at S226 in the Tg2576 mouse model of Alzheimer's disease.Experimental neurology · 2017Article
- Gene-body 5-hydroxymethylation is associated with gene expression changes in the prefrontal cortex of depressed individuals.Translational psychiatry · 2017Article
- Identification of Susceptible Loci and Enriched Pathways for Bipolar II Disorder Using Genome-Wide Association Studies.The international journal of neuropsychopharmacology · 2016Article
- Identification of Amino Acid Residues in Fibroblast Growth Factor 14 (FGF14) Required for Structure-Function Interactions with Voltage-gated Sodium Channel Nav1.6.The Journal of biological chemistry · 2016Article
- Currently recognized genes for schizophrenia: High-resolution chromosome ideogram representation.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2016Article
- Recent progress in the genetics of diabetic microvascular complications.World journal of diabetes · 2015Review
- Identifying a kinase network regulating FGF14:Nav1.6 complex assembly using split-luciferase complementation.PloS one · 2015Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
We previously reported linkage of schizophrenia and schizoaffective disorder to 13q32-34 in the European descent Afrikaner population from South Africa. The nature of genetic variation underlying linkage peaks in psychiatric disorders remains largely unknown and both rare and common variants may be contributing. Here, we examine the contribution of common variants located under the 13q32-34 linkage region. We used densely spaced SNPs to fine map the linkage peak region using both a discovery sample of 415 families and a meta-analysis incorporating two additional replication family samples. In a second phase of the study, we use one family-based data set with 237 families and independent case-control data sets for fine mapping of the common variant association signal using HapMap SNPs. We report a significant association with a genetic variant (rs9583277) within the gene encoding for the myosin heavy-chain Myr 8 (MYO16), which has been implicated in neuronal phosphoinositide 3-kinase signaling. Follow-up analysis of HapMap variation within MYO16 in a second set of Afrikaner families and additional case-control data sets of European descent highlighted a region across introns 2-6 as the most likely region to harbor common MYO16 risk variants. Expression analysis revealed a significant increase in the level of MYO16 expression in the brains of schizophrenia patients. Our results suggest that common variation within MYO16 may contribute to the genetic liability to schizophrenia.
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