β-Arrestins and Cell Signaling

By S. Dewire, Seungkirl Ahn, R. J. Lefkowitz, Sudha K. Shenoy. 2007

1,257 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/4b7e80080c14dc6719eee74e17bfbb04a2d64e2d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. S. Rajagopal
2. K. Rajagopal
3. Bryan L. Roth
4. R. J. Lefkowitz

In Molecular Biology

1. S. Rajagopal
2. R. J. Lefkowitz
3. K. Rajagopal
4. S. Dewire
5. Bryan L. Roth
6. Sudha K. Shenoy

Citations in the corpus

• A G Protein-Biased Ligand at the μ-Opioid Receptor Is Potently Analgesic with Reduced Gastrointestinal and Respiratory Dysfunction Compared with Morphine (2013, background): “…(Spengler et al., 1993; Eason et al., 1994), and between G protein coupling and b-arrestin recruitment (Azzi et al., 2003; Gesty-Palmer et al., 2006; DeWire et al., 2007; Violin and Lefkowitz, 2007; Kim et al., 2008; Ma et al., 2009; Gesty-Palmer and Luttrell, 2011; Rosethorne and Charlton, 2011).”
• Stress-Induced p38 Mitogen-Activated Protein Kinase Activation Mediates κ-Opioid-Dependent Dysphoria (2007, background): “KOR-mediated p38 activation, KOR-mediated aversion, and KOR-mediated swim stress-induced immobility are Gprotein-coupled receptor kinase-3 dependent Previous in vitro studies suggest that GPCR activation of MAPK may require -arrestin recruitment (Shenoy and Lefkowitz, 2005; Dewire et al., 2007).”
• Estrogen signaling through the transmembrane G protein-coupled receptor GPR30. (2008, background): “Arrestins are also capable of scaffolding a large number of signaling molecules, including, for example, mitogenactivated protein kinases (MAPKs), resulting in their G protein–independent activation and distinct subcellular localization (54).”
• Signalling ballet in space and time (2010, neutral): “The first is β-arrestin, a scaffold that coordinates the activation of multiple signalling pathways downstream of G-protein coupled receptors (GPCRs”
• Teaching old receptors new tricks: biasing seven-transmembrane receptors (2010, background): “This new perspective on 7TMR signalling represented a paradigm shif”
• Complement System Part II: Role in Immunity (2015, background): “This internalization of GPCR has already been demonstrated in in vitro assays as essential for the induction of the late stage of ERK signaling (119, 120).”
• DREADDs for Neuroscientists (2016, background): “This diminished response might be predicted because it is well known that GPCRs can be desensitized and subsequently internalized and downregulated following agonist-induced activation (DeWire et al., 2007).”
• Complement System Part I – Molecular Mechanisms of Activation and Regulation (2015, background): “This internalization is essential for the induction of the late stage of ERK signaling (291, 292).”