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Chen L et al. – Regulation of 5–HT1BR by GSK3 changed the dynamics of agonist–induced cell surface receptor internalization, in which lack of phosphorylation at S154 resulted in sustained reduction of 5–HT1BR at cell surface. Although the physiological consequences of selective regulation of 5–HT1BR by GSK3 remain to be identified, findings in this study reveal a new function of GSK3 as a protein kinase that is able to selectively regulate G protein–coupled receptors.

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