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dc.contributor.authorMartin, Pierre-Marieen_US
dc.contributor.authorStanley, Robert E.en_US
dc.contributor.authorRoss, Adam P.en_US
dc.contributor.authorFreitas, Andiara E.en_US
dc.contributor.authorMoyer, Caitlin E.en_US
dc.contributor.authorBrumback, Audrey C.en_US
dc.contributor.authorIafrati, Jillianen_US
dc.contributor.authorStapornwongkul, Kristina S.en_US
dc.contributor.authorDominguez, Skyen_US
dc.contributor.authorKivimäe, Saulen_US
dc.contributor.authorMulligan, Kimberly A.en_US
dc.contributor.authorPirooznia, Mehdien_US
dc.contributor.authorMcCombie, W. Richarden_US
dc.contributor.authorPotash, James B.en_US
dc.contributor.authorZandi, Peter P.en_US
dc.contributor.authorPurcell, Shaun M.en_US
dc.contributor.authorSanders, Stephan J.en_US
dc.contributor.authorZuo, Yien_US
dc.contributor.authorSohal, Vikaas S.en_US
dc.contributor.authorCheyette, Benjamin N.R.en_US
dc.date.accessioned2017-05-01T19:27:10Z
dc.date.issued2016en_US
dc.identifier.citationMartin, P., R. E. Stanley, A. P. Ross, A. E. Freitas, C. E. Moyer, A. C. Brumback, J. Iafrati, et al. 2016. “DIXDC1 contributes to psychiatric susceptibility by regulating dendritic spine and glutamatergic synapse density via GSK3 and Wnt/β-catenin signaling.” Molecular psychiatry :10.1038/mp.2016.184. doi:10.1038/mp.2016.184. http://dx.doi.org/10.1038/mp.2016.184.en
dc.identifier.issnen
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:32630523
dc.description.abstractMice lacking DIX domain containing-1 (DIXDC1), an intracellular Wnt/β-catenin signal pathway protein, have abnormal measures of anxiety, depression and social behavior. Pyramidal neurons in these animals’ brains have reduced dendritic spines and glutamatergic synapses. Treatment with lithium or a Glycogen Synthase Kinase-3 (GSK3) inhibitor corrects behavioral and neurodevelopmental phenotypes in these animals. Analysis of DIXDC1 in over 9,000 cases of autism, bipolar disorder and schizophrenia reveals higher rates of rare inherited sequence-disrupting single nucleotide variants (SNVs) in these individuals compared to psychiatrically-unaffected controls. Many of these SNVs alter Wnt/β-catenin signaling activity of the neurally-predominant DIXDC1 isoform; a subset that hyperactivate this pathway cause dominant neurodevelopmental effects. We propose that rare missense SNVs in DIXDC1 contribute to psychiatric pathogenesis by reducing spine and glutamatergic synapse density downstream of GSK3 in the Wnt/β-catenin pathway.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1038/mp.2016.184en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5395363/pdf/en
dash.licenseLAAen_US
dc.titleDIXDC1 contributes to psychiatric susceptibility by regulating dendritic spine and glutamatergic synapse density via GSK3 and Wnt/β-catenin signalingen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalMolecular psychiatryen
dc.date.available2017-05-01T19:27:10Z
dc.identifier.doi10.1038/mp.2016.184*
dash.authorsorderedfalse


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