<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kim J</submitter><funding>NICHD NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>Howard Hughes Medical Institute</funding><funding>National Heart, Lung, and Blood Institute</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><pagination>39</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6309084</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>β&lt;sub>2&lt;/sub>-adrenergic receptors (β&lt;sub>2&lt;/sub>ARs) are the target of catecholamines and play fundamental roles in cardiovascular, pulmonary, and skeletal muscle physiology. An important action of β&lt;sub>2&lt;/sub>AR stimulation on skeletal muscle is anabolic growth, which has led to the use of agonists such as clenbuterol by athletes to enhance muscle performance. While previous work has demonstrated that β&lt;sub>2&lt;/sub>ARs can engage distinct signaling and functional cascades mediated by either G proteins or the multifunctional adaptor protein, β-arrestin, the precise role of β-arrestin in skeletal muscle physiology is not known. Here, we tested the hypothesis that agonist activation of the β&lt;sub>2&lt;/sub>AR by clenbuterol would engage β-arrestin as a key transducer of anabo</pubmed_abstract><journal>Skeletal muscle</journal><pubmed_title>β-arrestin 1 regulates β2-adrenergic receptor-mediated skeletal muscle hypertrophy and contractility.</pubmed_title><pmcid>PMC6309084</pmcid><funding_grant_id>P01 HL075443</funding_grant_id><funding_grant_id>HD070872</funding_grant_id><funding_grant_id>R01-CA172570</funding_grant_id><funding_grant_id>K08 HL133488</funding_grant_id><funding_grant_id>R01 CA172570</funding_grant_id><funding_grant_id>K12 CA100639</funding_grant_id><funding_grant_id>HL056687</funding_grant_id><funding_grant_id>HL133488</funding_grant_id><funding_grant_id>R01 HL056687</funding_grant_id><funding_grant_id>HL16037</funding_grant_id><funding_grant_id>R01 DK109911</funding_grant_id><funding_grant_id>R01 HL016037</funding_grant_id><funding_grant_id>DK109911</funding_grant_id><funding_grant_id>5K12-CA100639-08</funding_grant_id><funding_grant_id>K08 HD070872</funding_grant_id><funding_grant_id>None</funding_grant_id><funding_grant_id>HL075443</funding_grant_id><pubmed_authors>Li T</pubmed_authors><pubmed_authors>Chen M</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Grotegut CA</pubmed_authors><pubmed_authors>Rosenberg PB</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Lefkowitz RJ</pubmed_authors><pubmed_authors>Wisler JW</pubmed_authors><pubmed_authors>Mao L</pubmed_authors><pubmed_authors>Rockman HA</pubmed_authors></additional><is_claimable>false</is_claimable><name>β-arrestin 1 regulates β2-adrenergic receptor-mediated skeletal muscle hypertrophy and contractility.</name><description>&lt;h4>Background&lt;/h4>β&lt;sub>2&lt;/sub>-adrenergic receptors (β&lt;sub>2&lt;/sub>ARs) are the target of catecholamines and play fundamental roles in cardiovascular, pulmonary, and skeletal muscle physiology. An important action of β&lt;sub>2&lt;/sub>AR stimulation on skeletal muscle is anabolic growth, which has led to the use of agonists such as clenbuterol by athletes to enhance muscle performance. While previous work has demonstrated that β&lt;sub>2&lt;/sub>ARs can engage distinct signaling and functional cascades mediated by either G proteins or the multifunctional adaptor protein, β-arrestin, the precise role of β-arrestin in skeletal muscle physiology is not known. Here, we tested the hypothesis that agonist activation of the β&lt;sub>2&lt;/sub>AR by clenbuterol would engage β-arrestin as a key transducer of anabo</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Dec</publication><modification>2025-04-21T21:33:47.838Z</modification><creation>2019-03-26T22:33:50Z</creation></dates><accession>S-EPMC6309084</accession><cross_references><pubmed>30591079</pubmed><doi>10.1186/s13395-018-0184-8</doi></cross_references></HashMap>