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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2015,2,17]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    Almost 20% of women and 40% of men in the United States abuse alcohol or have experienced alcohol dependence in their lifetime. Though accidents, traffic fatalities, and violent crimes account for the majority of alcohol-involved mortalities, excessive, chronic drinking also causes often irreversible heart and liver damage. We identify regulator of G protein signaling 6 (RGS6) as a novel drug target with substantive potential clinical utility in the treatment of alcoholism and amelioration of the resultant hepatic and cardiac toxicity. Mice lacking RGS6 exhibit a reduction in voluntary alcohol consumption, conditioned reward and withdrawal. In addition,\n                    <jats:italic>RGS6<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice are largely protected from alcohol-induced cardiomyopathy, hepatic steatosis, gastrointestinal barrier dysfunction, and endotoxemia. Thus, targeting RGS6 could reduce alcohol cravings while simultaneously protecting the heart and liver from damage.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1418795112","type":"journal-article","created":{"date-parts":[[2015,2,2]],"date-time":"2015-02-02T23:18:45Z","timestamp":1422919125000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":51,"title":["Regulator of G protein signaling 6 is a critical mediator of both reward-related behavioral and pathological responses to alcohol"],"prefix":"10.1073","volume":"112","author":[{"given":"Adele","family":"Stewart","sequence":"first","affiliation":[{"name":"Department of Pharmacology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Biswanath","family":"Maity","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon 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