ArticleNeuroscience2013
Effects of the Ras homolog Rhes on Akt/protein kinase B and glycogen synthase kinase 3 phosphorylation in striatum.
Article in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Rasd2 Mediates Acute Fasting-Induced Antidepressant-Like Effects via Dopamine D2 Receptor Activation in Ovariectomized Mice.The international journal of neuropsychopharmacology · 2023Article
- The identities of insulin signaling pathway are affected by overexpression of Tau and its phosphorylation form.Frontiers in aging neuroscience · 2022Article
- Involvement of the Protein Ras Homolog Enriched in the Striatum, Rhes, in Dopaminergic Neurons' Degeneration: Link to Parkinson's Disease.International journal of molecular sciences · 2021Review
- D1R- and D2R-Medium-Sized Spiny Neurons Diversity: Insights Into Striatal Vulnerability to Huntington's Disease Mutation.Frontiers in cellular neuroscience · 2021Review
- Article
- Decreased Rhes mRNA levels in the brain of patients with Parkinson's disease and MPTP-treated macaques.PloS one · 2017Article
- RasGRP1 promotes amphetamine-induced motor behavior through a Rhes interaction network ("Rhesactome") in the striatum.Science signaling · 2016Article
- Therapeutic Mechanisms of Lithium in Bipolar Disorder: Recent Advances and Current Understanding.CNS drugs · 2016Review
- Rasd2 Modulates Prefronto-Striatal Phenotypes in Humans and 'Schizophrenia-Like Behaviors' in Mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Dopamine D2 receptors' effects on renal inflammation are mediated by regulation of PP2A function.American journal of physiology. Renal physiology · 2016Article
- 4-Phenylbutyric Acid (4-PBA) and Lithium Cooperatively Attenuate Cell Death during Oxygen-Glucose Deprivation (OGD) and Reoxygenation.Cellular and molecular neurobiology · 2015Article
- Rhes influences striatal cAMP/PKA-dependent signaling and synaptic plasticity in a gender-sensitive fashion.Scientific reports · 2015Article
- Impaired TrkB receptor signaling underlies corticostriatal dysfunction in Huntington's disease.Neuron · 2014Article
- Activators of G protein signaling exhibit broad functionality and define a distinct core signaling triad.Molecular pharmacology · 2014Review
- Rhes, a striatal-selective protein implicated in Huntington disease, binds beclin-1 and activates autophagy.The Journal of biological chemistry · 2014Article
- Preclinical and clinical investigations of mood stabilizers for Huntington's disease: what have we learned?International journal of biological sciences · 2014Review
- PKA modulates iron trafficking in the striatum via small GTPase, Rhes.Neuroscience · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
G protein-coupled receptors (GPCR) signal not only through heterotrimeric G proteins, but also through alternate pathways. Thus, dopamine D2 receptors in the striatum signal through Gαi/o and also by promoting formation of a multi-protein complex containing β-arrestin2, protein phosphatase 2A (PP2A), and Akt in order to dephosphorylate Akt. Lithium, on the other hand, disrupts this complex to increase Akt phosphorylation. Rhes is a striatally enriched GTP-binding protein that has been shown to inhibit dopamine receptor-mediated behavior and signaling through heterotrimeric G proteins. Therefore, our objective was to test whether Rhes similarly affects signaling through the Akt/GSK3 pathway in the striatum. Rhes(-/-) mice showed basally increased Akt and GSK3β phosphorylation relative to rhes(+/+) mice that was not further enhanced by lithium treatment. Furthermore, they responded to the D1/D2 agonist apomorphine with increased Akt and GSK3 phosphorylation. Co-immunoprecipitation experiments revealed that apomorphine treatment recruits PP 2A-C to Akt in both rhes(+/+) and rhes(-/-) mice. Lithium did not disrupt their interaction in rhes(-/-) mice as there was little basal interaction. Rhes co-immunoprecipitated with β-arrestins, suggesting that it is integral to the multi-protein complex. Thus, Rhes is necessary for Akt dephosphorylation by the striatal multi-protein complex, and in its absence, a lithium-treated phenotype results.
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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.