Independent β-arrestin 2 and G protein-mediated pathways for angiotensin II activation of extracellular signal-regulated kinases 1 and 2

By Huijun Wei, Seungkirl Ahn, Sudha K. Shenoy, S. Karnik, L. Hunyady, L. Luttrell, R. J. Lefkowitz. Proceedings of the National Academy of Sciences of the United States of America, 2003

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Coordinating ERK/MAPK signalling through scaffolds and inhibitors (2005, background): “GPCRs that only bind transiently to β-arrestin-2 generate less activated ERK/MAPK, but permit stronger nuclear signallin”
Teaching old receptors new tricks: biasing seven-transmembrane receptors (2010, background): “These include SII angiotensin (Sar 1 , Ile 4 , Ile 8”
A G Protein-Biased Ligand at the μ-Opioid Receptor Is Potently Analgesic with Reduced Gastrointestinal and Respiratory Dysfunction Compared with Morphine (2013, background): “This is consistent with the understanding that b-arrestins not only desensitize a receptor’s G protein-mediated signaling but also stimulate distinct and independent cell-signaling outcomes (Wei et al., 2003; Rajagopal et al., 2006; Gesty-Palmer et al., 2009; Violin et al., 2010; Allen et al., 2011;”