<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Srinivasan C</submitter><funding>Carnegie Mellon Computational Biology Department Lane Postdoctoral Fellowship</funding><funding>NIDA NIH HHS</funding><funding>HHS | NIH | National Institute of General Medical Sciences</funding><funding>Carnegie Mellon Brainhub Presidential Fellowship</funding><funding>HHS | NIH | National Institute on Drug Abuse</funding><funding>Alfred P. Sloan Foundation</funding><funding>NIGMS NIH HHS</funding><funding>National Science Foundation</funding><pagination>9008-9030</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8549541</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(43)</volume><pubmed_abstract>Recent large genome-wide association studies have identified multiple confident risk loci linked to addiction-associated behavioral traits. Most genetic variants linked to addiction-associated traits lie in noncoding regions of the genome, likely disrupting &lt;i>cis&lt;/i>-regulatory element (CRE) function. CREs tend to be highly cell type-specific and may contribute to the functional development of the neural circuits underlying addiction. Yet, a systematic approach for predicting the impact of risk variants on the CREs of specific cell populations is lacking. To dissect the cell types and brain regions underlying addiction-associated traits, we applied stratified linkage disequilibrium score regression to compare genome-wide association studies to genomic regions collected from human and mous</pubmed_abstract><journal>The Journal of neuroscience : the official journal of the Society for Neuroscience</journal><pubmed_title>Addiction-Associated Genetic Variants Implicate Brain Cell Type- and Region-Specific Cis-Regulatory Elements in Addiction Neurobiology.</pubmed_title><pmcid>PMC8549541</pmcid><funding_grant_id>DP1 DA046585</funding_grant_id><funding_grant_id>1DP1DA046585</funding_grant_id><funding_grant_id>DGE1745016</funding_grant_id><funding_grant_id>F30 DA053020</funding_grant_id><funding_grant_id>T32GM008208</funding_grant_id><funding_grant_id>F30DA053020</funding_grant_id><funding_grant_id>T32 GM008208</funding_grant_id><pubmed_authors>Phan BN</pubmed_authors><pubmed_authors>Ramamurthy E</pubmed_authors><pubmed_authors>Lawler AJ</pubmed_authors><pubmed_authors>Brown AR</pubmed_authors><pubmed_authors>Srinivasan C</pubmed_authors><pubmed_authors>Kleyman M</pubmed_authors><pubmed_authors>Kaplow IM</pubmed_authors><pubmed_authors>Wirthlin ME</pubmed_authors><pubmed_authors>Pfenning AR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Addiction-Associated Genetic Variants Implicate Brain Cell Type- and Region-Specific Cis-Regulatory Elements in Addiction Neurobiology.</name><description>Recent large genome-wide association studies have identified multiple confident risk loci linked to addiction-associated behavioral traits. Most genetic variants linked to addiction-associated traits lie in noncoding regions of the genome, likely disrupting &lt;i>cis&lt;/i>-regulatory element (CRE) function. CREs tend to be highly cell type-specific and may contribute to the functional development of the neural circuits underlying addiction. Yet, a systematic approach for predicting the impact of risk variants on the CREs of specific cell populations is lacking. To dissect the cell types and brain regions underlying addiction-associated traits, we applied stratified linkage disequilibrium score regression to compare genome-wide association studies to genomic regions collected from human and mous</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2026-06-17T06:24:16.085Z</modification><creation>2025-02-19T01:26:08.985Z</creation></dates><accession>S-EPMC8549541</accession><cross_references><pubmed>34462306</pubmed><doi>10.1523/JNEUROSCI.2534-20.2021</doi></cross_references></HashMap>