Beta-arrestins and cell signaling.

706 citations recorded by the source corpus.

How researchers see this paper

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

Stress-Induced p38 Mitogen-Activated Protein Kinase Activation Mediates κ-Opioid-Dependent Dysphoria (2007, background): “The role of G-protein-coupled receptor phosphorylation by GRK in signaling has recently gained attention, because it has been shown that sustained agonist occupation and subsequent phosphorylation of the receptor can alter coupling to the MAPK signaling cassette in vitro (Shenoy and Lefkowitz, 2005;”
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).”
β-arrestin-mediated receptor trafficking and signal transduction (2011, background): “Upon agonist-stimulation, many 7TMRs induce translocation of cytosolic β-arrestins to the plasma membrane, which can occur even in the absence of G protein activation and can be visualized by monitoring Green Fluorescent Protein (GFP)-β-arrestin [29,30].”