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However, it is possible that bias towards G-protein signaling may stem more from reduced activation of G-protein-coupled receptor kinases than inhibition of binding to beta-arrestins, while other studies have shown that certain β2AR ligands prefer beta-arrestin signaling over G-protein activation [23,24]

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The researchers concluded that there may be other determinants, such as tissue-specific cofactors, negative feedback loops, and epigenetic or signalling mechanisms, which affect both basal expression and Nrf2-mediated transcriptional regulation of these highly expressed genes in cells [116]