<I>β</I>-Arrestin-Mediated Signaling Improves the Efficacy of Therapeutics

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  • Ibrahim Islam A.A.E.-H.
    Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan Department of Pharmacology, Faculty of Pharmacy, Zagazig University, Egypt Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan Department of Pharmacology, Faculty of Pharmacy, Zagazig University, Egypt
  • Kurose Hitoshi
    Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan

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  • Current Perspective : β-Arrestin-Mediated Signaling Improves the Efficacy of Therapeutics
  • β-Arrestin-Mediated Signaling Improves the Efficacy of Therapeutics

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Abstract

β-Arrestins (β-arrestin-1 and β-arrestin-2) were first identified as proteins that have the ability to desensitize G protein-coupled receptors (GPCRs). However, it has recently been found that β-arrestins can activate signaling pathways independent of G protein activation. The diversity of these signaling pathways has also been recognized. This leads to an appreciation of β-arrestin-biased agonists, which is a new class of drugs that selectively activate β-arrestin-mediated signaling without G protein activation. In this review, we will discuss the recent advance of β-arrestin-mediated signaling pathways, including a brief account of different biased agonists, their pharmacological applications, and novel β-arrestin research.

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