Title : G protein-coupled receptor kinases (GRKs) orchestrate biased agonism at the β2-adrenergic receptor.

Pub. Date : 2018 Aug 21

PMID : 30131371






2 Functional Relationships(s)
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1 We showed that an alanine mutant of the highly conserved residue tyrosine 219 (Y219A) in transmembrane domain five of the beta2-adrenergic receptor (beta2AR) was incapable of beta-arrestin recruitment, receptor internalization, and beta-arrestin-mediated activation of extracellular signal-regulated kinase (ERK), whereas it retained the ability to signal through G protein. Tyrosine mitogen-activated protein kinase 1 Homo sapiens
2 We showed that an alanine mutant of the highly conserved residue tyrosine 219 (Y219A) in transmembrane domain five of the beta2-adrenergic receptor (beta2AR) was incapable of beta-arrestin recruitment, receptor internalization, and beta-arrestin-mediated activation of extracellular signal-regulated kinase (ERK), whereas it retained the ability to signal through G protein. Tyrosine mitogen-activated protein kinase 1 Homo sapiens