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dc.contributor.authorLaVigne, Justin
dc.contributor.authorKeresztes, Attila
dc.contributor.authorChiem, Daniel
dc.contributor.authorStreicher, John M
dc.date.accessioned2020-05-04T18:02:14Z
dc.date.available2020-05-04T18:02:14Z
dc.date.issued2020-04
dc.identifier.citationLaVigne, J., Keresztes, A., Chiem, D. et al. The endomorphin-1/2 and dynorphin-B peptides display biased agonism at the mu opioid receptor. Pharmacol. Rep 72, 465–471 (2020). https://doi.org/10.1007/s43440-020-00061-xen_US
dc.identifier.issn1734-1140
dc.identifier.pmid32112361
dc.identifier.doi10.1007/s43440-020-00061-x
dc.identifier.urihttp://hdl.handle.net/10150/641157
dc.description.abstractDynorphins, enkephalins, and endomorphins are endogenous opioid agonist peptides that may possess distinct bias profiles; biased agonism of endogenous peptides could explain the selective roles of these ligands in vivo. Our purpose in the present study was to investigate biased signaling and potential underlying molecular mechanisms of bias using 35S-GTPγS and cAMP assays, specifically focusing on the role of adenylyl cyclases (ACs) and regulators of G-protein signaling proteins (RGSs) in CHO, N2a, and SH-SY5Y cell lines, all expressing the human MOR.en_US
dc.language.isoenen_US
dc.publisherSPRINGER HEIDELBERGen_US
dc.rightsCopyright © 2020, Springer Nature.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subject35S-GTPγS couplingen_US
dc.subjectBiased agonismen_US
dc.subjectEndogenous opioid peptidesen_US
dc.subjectEndomorphinen_US
dc.subjectForskolin-stimulated cAMP accumulationen_US
dc.titleThe endomorphin-1/2 and dynorphin-B peptides display biased agonism at the mu opioid receptoren_US
dc.typeArticleen_US
dc.contributor.departmentUniv Arizona, Coll Med, Dept Pharmacolen_US
dc.identifier.journalPHARMACOLOGICAL REPORTSen_US
dc.description.note12 month embargo; published online: 28 February 2020en_US
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en_US
dc.eprint.versionFinal accepted manuscripten_US
dc.source.journaltitlePharmacological reports : PR
dc.source.volume72
dc.source.issue2
dc.source.beginpage465
dc.source.endpage471
dc.source.countrySwitzerland


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