ArticleThe Journal of biological chemistry2011
Rapid dephosphorylation of G protein-coupled receptors by protein phosphatase 1β is required for termination of β-arrestin-dependent signaling.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Altered Intracellular Trafficking as a Mechanism for Prolonged Duration of G Protein-Coupled Receptor Activation.Journal of the American Chemical Society · 2026Article
- Short-chain fatty acids: key antiviral mediators of gut microbiota.Frontiers in immunology · 2025Review
- SZ-685C inhibits the growth of non-functioning pituitary adenoma by down-regulating miR-340-3p and inducing autophagy.Heliyon · 2024Article
- In situ visualization of opioid and cannabinoid drug effects using phosphosite-specific GPCR antibodies.Communications biology · 2023Article
- Agonist-induced phosphorylation bar code and differential post-activation signaling of the delta opioid receptor revealed by phosphosite-specific antibodies.Scientific reports · 2020Article
- Encoding the β-Arrestin Trafficking Fate of Ghrelin Receptor GHSR1a: C-Tail-Independent Molecular Determinants in GPCRs.ACS pharmacology & translational science · 2019Article
- Regulation of heterologously expressed 5-HTBritish journal of pharmacology · 2019Article
- International Union of Basic and Clinical Pharmacology. CV. Somatostatin Receptors: Structure, Function, Ligands, and New Nomenclature.Pharmacological reviews · 2018Review
- Functional Amyloids and their Possible Influence on Alzheimer Disease.Discoveries (Craiova, Romania) · 2017Review
- The heterotrimeric G protein GβThe Journal of biological chemistry · 2017Article
- Identification of Phosphorylation Sites Regulating sst3 Somatostatin Receptor Trafficking.Molecular endocrinology (Baltimore, Md.) · 2016Article
- Fine-tuning somatostatin receptor signalling by agonist-selective phosphorylation and dephosphorylation: IUPHAR Review 5.British journal of pharmacology · 2014Review
- Heterologous regulation of agonist-independent μ-opioid receptor phosphorylation by protein kinase C.British journal of pharmacology · 2014Article
- Differential regulation of somatostatin receptor dephosphorylation by β-arrestin1 and β-arrestin2.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- Mechanisms of regulation of olfactory transduction and adaptation in the olfactory cilium.PloS one · 2014Article
- Article
- Illuminating somatostatin analog action at neuroendocrine tumor receptors.Trends in pharmacological sciences · 2013Review
- Phosphorylation of threonine 333 regulates trafficking of the human sst5 somatostatin receptor.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Differentiation of opioid drug effects by hierarchical multi-site phosphorylation.Molecular pharmacology · 2013Article
- Deciphering µ-opioid receptor phosphorylation and dephosphorylation in HEK293 cells.British journal of pharmacology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Termination of signaling of activated G protein-coupled receptors (GPCRs) is essential for maintenance of cellular homeostasis. It is well established that β-arrestin redistributes to phosphorylated GPCRs and thereby facilitates desensitization of classical G protein-dependent signaling. β-Arrestin in turn serves as a scaffold to initiate a second wave of signaling. Here, we report a molecular mechanism that regulates the termination of unconventional β-arrestin-dependent GPCR signaling. We identify protein phosphatase 1β (PP1β) as a phosphatase for the cluster of phosphorylated threonines ((353)TTETQRT(359)) within the sst(2A) somatostatin receptor carboxyl terminus that mediates β-arrestin binding using siRNA knock-down screening. We show that PP1β-mediated sst(2A) dephosphorylation is initiated directly after receptor activation at or near the plasma membrane. As a functional consequence of diminished PP1β activity, we find that somatostatin- and substance P-induced but not epidermal growth factor-induced ERK activation was aberrantly enhanced and prolonged. Thus, we demonstrate a novel mechanism for fine tuning unconventional β-arrestin-dependent GPCR signaling in that recruitment of PP1β to activated GPCRs facilitates GPCR dephosphorylation and, hence, leads to disruption of the β-arrestin-GPCR complex.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.