<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gardner OK</submitter><funding>NCATS NIH HHS</funding><funding>NIA NIH HHS</funding><funding>National Institutes of Health</funding><funding>National Institute on Aging</funding><pagination>2876-2886</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9433728</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(17)</volume><pubmed_abstract>Most Alzheimer's disease (AD)-associated genetic variants do not change protein coding sequence and thus likely exert their effects through regulatory mechanisms. RNA editing, the post-transcriptional modification of RNA bases, is a regulatory feature that is altered in AD patients that differs across ancestral backgrounds. Editing QTLs (edQTLs) are DNA variants that influence the level of RNA editing at a specific site. To study the relationship of DNA variants genome-wide, and particularly in AD-associated loci, with RNA editing, we performed edQTL analyses in self-reported individuals of African American (AF) or White (EU) race with corresponding global genetic ancestry averaging 82.2% African ancestry (AF) and 96.8% European global ancestry (EU) in the two groups, respectively. We used</pubmed_abstract><journal>Human molecular genetics</journal><pubmed_title>Genetic architecture of RNA editing regulation in Alzheimer's disease across diverse ancestral populations.</pubmed_title><pmcid>PMC9433728</pmcid><funding_grant_id>RF1 AG070935</funding_grant_id><funding_grant_id>AG027944</funding_grant_id><funding_grant_id>UL1 TR001420</funding_grant_id><funding_grant_id>AG028786</funding_grant_id><funding_grant_id>R01 AG070864</funding_grant_id><funding_grant_id>R01 AG072547</funding_grant_id><funding_grant_id>AG070935</funding_grant_id><funding_grant_id>R01 AG070935</funding_grant_id><funding_grant_id>R56 AG072547</funding_grant_id><funding_grant_id>U01 AG032984</funding_grant_id><funding_grant_id>R01 AG027944</funding_grant_id><funding_grant_id>U01AG052410-01</funding_grant_id><funding_grant_id>R01 AG028786</funding_grant_id><funding_grant_id>AG072547</funding_grant_id><funding_grant_id>U01 AG052410</funding_grant_id><funding_grant_id>AG070864</funding_grant_id><pubmed_authors>Gu T</pubmed_authors><pubmed_authors>Adams LD</pubmed_authors><pubmed_authors>Starks TD</pubmed_authors><pubmed_authors>Vance JM</pubmed_authors><pubmed_authors>Nuytemans K</pubmed_authors><pubmed_authors>Martin ER</pubmed_authors><pubmed_authors>Byrd GS</pubmed_authors><pubmed_authors>Griswold AJ</pubmed_authors><pubmed_authors>Haines JL</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Cuccaro ML</pubmed_authors><pubmed_authors>Pericak-Vance MA</pubmed_authors><pubmed_authors>Bush WS</pubmed_authors><pubmed_authors>Beecham GW</pubmed_authors><pubmed_authors>Hofmann NK</pubmed_authors><pubmed_authors>Hamilton-Nelson KL</pubmed_authors><pubmed_authors>Van Booven D</pubmed_authors><pubmed_authors>Whitehead PL</pubmed_authors><pubmed_authors>Gardner OK</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic architecture of RNA editing regulation in Alzheimer's disease across diverse ancestral populations.</name><description>Most Alzheimer's disease (AD)-associated genetic variants do not change protein coding sequence and thus likely exert their effects through regulatory mechanisms. RNA editing, the post-transcriptional modification of RNA bases, is a regulatory feature that is altered in AD patients that differs across ancestral backgrounds. Editing QTLs (edQTLs) are DNA variants that influence the level of RNA editing at a specific site. To study the relationship of DNA variants genome-wide, and particularly in AD-associated loci, with RNA editing, we performed edQTL analyses in self-reported individuals of African American (AF) or White (EU) race with corresponding global genetic ancestry averaging 82.2% African ancestry (AF) and 96.8% European global ancestry (EU) in the two groups, respectively. We used</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2026-05-09T03:12:03.329Z</modification><creation>2025-02-19T02:38:07.514Z</creation></dates><accession>S-EPMC9433728</accession><cross_references><pubmed>35383839</pubmed><doi>10.1093/hmg/ddac075</doi></cross_references></HashMap>