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Despite the canonical role of β-arrestins in clathrin-mediated endocytosis, it does not appear that the deficient β-arrestin response of biased agonists is directly responsible for the their distinct trafficking profiles, as agonist-induced GLP-1R endocytosis is minimally affected by the total absence of both β-arrestin isoforms (87)
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Combined receptor activity quiets hunger more reliably than GLP-1 alone
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