<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li M</submitter><funding>NICHD NIH HHS</funding><funding>NIA NIH HHS</funding><funding>Medical Research Council</funding><funding>NINDS NIH HHS</funding><funding>Lundbeck Foundation</funding><pagination>452-61</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3937299</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(4)</volume><pubmed_abstract>Bipolar disorder (BD) is a polygenic disorder that shares substantial genetic risk factors with major depressive disorder (MDD). Genetic analyses have reported numerous BD susceptibility genes, while some variants, such as single-nucleotide polymorphisms (SNPs) in CACNA1C have been successfully replicated, many others have not and subsequently their effects on the intermediate phenotypes cannot be verified. Here, we studied the MDD-related gene CREB1 in a set of independent BD sample groups of European ancestry (a total of 64,888 subjects) and identified multiple SNPs significantly associated with BD (the most significant being SNP rs6785[A], P=6.32 × 10(-5), odds ratio (OR)=1.090). Risk SNPs were then subjected to further analyses in healthy Europeans for intermediate phenotypes of BD, in</pubmed_abstract><journal>Molecular psychiatry</journal><pubmed_title>Allelic differences between Europeans and Chinese for CREB1 SNPs and their implications in gene expression regulation, hippocampal structure and function, and bipolar disorder susceptibility.</pubmed_title><pmcid>PMC3937299</pmcid><funding_grant_id>U24 AG021886</funding_grant_id><funding_grant_id>U01 AG049505</funding_grant_id><funding_grant_id>G9817803B</funding_grant_id><funding_grant_id>R01 NS017950</funding_grant_id><funding_grant_id>R155-2014-1724</funding_grant_id><funding_grant_id>P30 AG010129</funding_grant_id><funding_grant_id>R01 HD050735</funding_grant_id><funding_grant_id>R01 AG008122</funding_grant_id><pubmed_authors>Shi L</pubmed_authors><pubmed_authors>Lin Q</pubmed_authors><pubmed_authors>Su B</pubmed_authors><pubmed_authors>Martin NG</pubmed_authors><pubmed_authors>Cichon S</pubmed_authors><pubmed_authors>Rietschel M</pubmed_authors><pubmed_authors>Nothen MM</pubmed_authors><pubmed_authors>Gill M</pubmed_authors><pubmed_authors>Hibar DP</pubmed_authors><pubmed_authors>Medland SE</pubmed_authors><pubmed_authors>Jamain S</pubmed_authors><pubmed_authors>Ikram MA</pubmed_authors><pubmed_authors>Sullivan PF</pubmed_authors><pubmed_authors>Leboyer M</pubmed_authors><pubmed_authors>Walter H</pubmed_authors><pubmed_authors>CHARGE Consortium</pubmed_authors><pubmed_authors>Donohoe G</pubmed_authors><pubmed_authors>Corvin A</pubmed_authors><pubmed_authors>Debette S</pubmed_authors><pubmed_authors>Arias Vasquez A</pubmed_authors><pubmed_authors>Li M</pubmed_authors><pubmed_authors>Hargreaves A</pubmed_authors><pubmed_authors>Stein JL</pubmed_authors><pubmed_authors>Muller-Myhsok B</pubmed_authors><pubmed_authors>Luo XJ</pubmed_authors><pubmed_authors>Thompson PM</pubmed_authors><pubmed_authors>Fornage M</pubmed_authors><pubmed_authors>Hultman C</pubmed_authors><pubmed_authors>Morris DW</pubmed_authors><pubmed_authors>ENIGMA Consortium</pubmed_authors><pubmed_authors>Henry C</pubmed_authors><pubmed_authors>Franke B</pubmed_authors><pubmed_authors>Toga AW</pubmed_authors><pubmed_authors>Heinz A</pubmed_authors><pubmed_authors>Alzheimer’s Disease Neuroimaging Initiative</pubmed_authors><pubmed_authors>Czamara D</pubmed_authors><pubmed_authors>Mattheisen M</pubmed_authors><pubmed_authors>Bergen SE</pubmed_authors><pubmed_authors>MooDS Bipolar Consortium</pubmed_authors><pubmed_authors>Meyer-Lindenberg A</pubmed_authors><pubmed_authors>Lewis CM</pubmed_authors><pubmed_authors>Landen M</pubmed_authors><pubmed_authors>Wright MJ</pubmed_authors><pubmed_authors>Bellivier F</pubmed_authors><pubmed_authors>Swedish Bipolar Study Group</pubmed_authors><pubmed_authors>Seshadri S</pubmed_authors><pubmed_authors>Erk S</pubmed_authors><pubmed_authors>Etain B</pubmed_authors><pubmed_authors>Bis JC</pubmed_authors><pubmed_authors>Schulze TG</pubmed_authors><pubmed_authors>Gan L</pubmed_authors><pubmed_authors>Launer LJ</pubmed_authors><pubmed_authors>Shi H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Allelic differences between Europeans and Chinese for CREB1 SNPs and their implications in gene expression regulation, hippocampal structure and function, and bipolar disorder susceptibility.</name><description>Bipolar disorder (BD) is a polygenic disorder that shares substantial genetic risk factors with major depressive disorder (MDD). Genetic analyses have reported numerous BD susceptibility genes, while some variants, such as single-nucleotide polymorphisms (SNPs) in CACNA1C have been successfully replicated, many others have not and subsequently their effects on the intermediate phenotypes cannot be verified. Here, we studied the MDD-related gene CREB1 in a set of independent BD sample groups of European ancestry (a total of 64,888 subjects) and identified multiple SNPs significantly associated with BD (the most significant being SNP rs6785[A], P=6.32 × 10(-5), odds ratio (OR)=1.090). Risk SNPs were then subjected to further analyses in healthy Europeans for intermediate phenotypes of BD, in</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Apr</publication><modification>2026-05-04T09:06:27.033Z</modification><creation>2019-03-27T01:22:29Z</creation></dates><accession>S-EPMC3937299</accession><cross_references><pubmed>23568192</pubmed><doi>10.1038/mp.2013.37</doi></cross_references></HashMap>