β-arrestin-dependent activation of the ERK MAP kinase downstream of GPCRs typically originates from internalized receptor-β-arrestin-ERK complexes. A new study now reports that β-arrestin 2 is sufficiently 'primed' after 'kissing' the β1-adrenergic receptor to initiate ERK activation even in the absence of formation of the receptor-β-arrestin-ERK complex and receptor internalization.
Copyright © 2016 Elsevier Ltd. All rights reserved.