Regulation of receptor trafficking by GRKs and arrestins.
By C. C. Moore, S. Milano, J. Benovic. Annual Review of Physiology, 2007
705 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1178aa05128c5f1e67ee439a86c4e46e2280bc67
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In Cellular and Molecular Neuroscience
In Molecular Biology
Citations in the corpus
- β-arrestin-mediated receptor trafficking and signal transduction (2011, background): “Studies that characterized a direct interaction between β-arrestin1 and clathrin have shed light on the mechanisms by which β-arrestins promote 7TMR endocytosis [15].”
- Estrogen signaling through the transmembrane G protein-coupled receptor GPR30. (2008, background): “However, arrestin binding is now recognized to be an important mediator of receptor internalization through interactions with clathrin and AP-2 (53).”
- Arf Family G Proteins and their regulators: roles in membrane transport, development and disease (2011, background): “GIT1 and its substrate ARF6 affect ligand-stimulated endocytosis of several GPCRs through either clathrin-dependent or clathrin-independent endocytic pathways 119 .”
- Endocytosis and signalling: intertwining molecular networks (2009, neutral): “This adaptor function is promoted by the ligand-induced activation of receptors and by GPCR kinase-induced phosphorylation of cytoplasmic serine and threonine residues in the recepto”