ArticleMolecular pharmacology2009
Regulation of serotonin 1B receptor by glycogen synthase kinase-3.
Article in Molecular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Glycogen synthase kinase-3ß supports serotonin transporter function and trafficking in a phosphorylation-dependent manner.Journal of neurochemistry · 2021Article
- Glycogen synthase kinase-3 signaling in cellular and behavioral responses to psychostimulant drugs.Biochimica et biophysica acta. Molecular cell research · 2020Review
- 5-HTACS chemical neuroscience · 2019Article
- Regulation of heterologously expressed 5-HTBritish journal of pharmacology · 2019Article
- Article
- Modulation of Synaptic Plasticity in the Cortex Needs to Understand All the Players.Frontiers in synaptic neuroscience · 2017Review
- Fine-Tuning of the RIG-I-Like Receptor/Interferon Regulatory Factor 3-Dependent Antiviral Innate Immune Response by the Glycogen Synthase Kinase 3/β-Catenin Pathway.Molecular and cellular biology · 2015Article
- Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases.Pharmacology & therapeutics · 2015Review
- Focal adhesion kinase-mediated activation of glycogen synthase kinase 3β regulates IL-33 receptor internalization and IL-33 signaling.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Glycogen synthase kinase-3 as a therapeutic target for cognitive dysfunction in neuropsychiatric disorders.CNS drugs · 2015Review
- A PrP(C)-caveolin-Lyn complex negatively controls neuronal GSK3β and serotonin 1B receptor.Scientific reports · 2014Article
- A noncanonical postsynaptic transport route for a GPCR belonging to the serotonin receptor family.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Behavioral stress-induced activation of FoxO3a in the cerebral cortex of mice.Biological psychiatry · 2012Article
- A role for Akt and glycogen synthase kinase-3 as integrators of dopamine and serotonin neurotransmission in mental health.Journal of psychiatry & neuroscience : JPN · 2012Review
- Functional significance of glycogen synthase kinase-3 regulation by serotonin.Cellular signalling · 2012Article
- Article
- Review of pharmacological treatment in mood disorders and future directions for drug development.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Review
- Identification of a glycogen synthase kinase-3β inhibitor that attenuates hyperactivity in CLOCK mutant mice.ChemMedChem · 2011Article
- Regulation of dorsal raphe nucleus function by serotonin autoreceptors: a behavioral perspective.Journal of chemical neuroanatomy · 2011Review
- Glycogen synthase kinase-3β is a functional modulator of serotonin-1B receptors.Molecular pharmacology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In response to 5-hydroxytryptamine (5-HT), the type 1 serotonin receptors (5-HT1Rs) preferentially couple to the inhibitory G protein and elicit many physiological and behavioral processes. However, their regulation by intracellular protein kinases has not been fully investigated. In this study, we identified that glycogen synthase kinase-3 (GSK3) differentially regulates 5-HT1Rs. In receptor-expressing cells and brain slices, activation of both 5-HT1AR and 5-HT1BR reduced forskolin-stimulated cAMP production, but only the effect of 5-HT1BR was abolished by selective GSK3 inhibitors, deletion of GSK3beta by RNAi, or overexpression of impaired GSK3beta mutants (R96A and K85,86A). A consensus GSK3 phosphorylation sequence was identified between the serine-154 and threonine-158 in the second intracellular loop of 5-HT1BR. Mutation of either serine-154 or threonine-158 to alanine significantly reduced response of 5-HT1BR to 5-HT. Active GSK3beta interacted with resting 5-HT1BR to form a protein complex. The interaction was enhanced by receptor activation, abolished by GSK3 inhibitors, and dependent on the phosphorylation state of serine-154. In addition, regulation of 5-HT1BR by GSK3 changed the dynamics of agonist-induced cell surface receptor internalization, in which lack of phosphorylation at Ser154 resulted in sustained reduction of 5-HT1BR at the cell surface. Although the physiological consequences of selective regulation of 5-HT1BR by GSK3 remain to be identified, findings in this study reveal a new function of GSK3 as a protein kinase that is able to selectively regulate G protein-coupled receptors.
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Registered trials
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.