The role of beta-arrestins in the termination and transduction of G-protein-coupled receptor signals.
By L. Luttrell, R. J. Lefkowitz. Journal of Cell Science, 2002
1,232 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/83aeb8b0b525c41c7f5c962d7a061a72a7b34539
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Citations in the corpus
- The genetic design of signaling cascades to record receptor activation (2008, background): “Ligand-occupied phosphorylated receptor then recruits arrestin, preventing further G protein activation (7).”
- The Physiology, Signaling, and Pharmacology of Dopamine Receptors (2011, background): “However, accumulating evidence suggests that these receptors do not signal exclusively through heterotrimeric G proteins and may also engage in G proteinindependent signaling events (Luttrell et al., 1999; Luttrell and Lefkowitz, 2002).”
- Role of the CXCL8-CXCR1/2 Axis in Cancer and Inflammatory Diseases (2017, unknown): “β-arrestin1/2 association inhibits G-protein coupling of receptors and recruits the endocytic machinery such as clathrin and AP-2 to mediate receptor internalization and sequestration [70].”
- G Protein-Coupled Receptor Kinases (2016, background): “Cell Mol Life Sci 71(8):1529–1546 139.”
- GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. (2010, unknown): “GPCRs and couple the receptor to specific downstream signaling pathways, as well as mediate receptor endocytosis (Luttrell and Lefkowitz, 2002).”
- Desensitization of G protein-coupled receptors and neuronal functions. (2004, background): “Furthermore, GRKs and arrestins appear to play direct signaling roles (Hall et al. 1999, Luttrell & Lefkowitz 2002).”
- INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, unknown): “Activation of GPR120 by omega 3 FAs specifically inhibits TAK phosphorylation and activation, providing a mechanism for the broad inhibition of Tlr and TNF signaling (Oh et al., 2010). b arrestins are a family of molecules that can serve as adaptor or scaffold proteins for a number of different GPCR”