ArticleOncogene2004
The small GTP-binding protein, Rhes, regulates signal transduction from G protein-coupled receptors.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 107 citations in OpenAlex.
- RASD2 Drives Renal Clear Cell Carcinoma Progression via RAF1 (Ser338) Phosphorylation.Cancer science · 2026Article
- Rasd2 regulates depression-like behaviors via DRD2 neurons in the prelimbic cortex afferent to nucleus accumbens core circuit.Molecular psychiatry · 2025Article
- Rhes, a striatal enriched protein, regulates post-translational small-ubiquitin-like-modifier (SUMO) modification of nuclear proteins and alters gene expression.Cellular and molecular life sciences : CMLS · 2024Article
- Curbing Rhes Actions: Mechanism-based Molecular Target for Huntington's Disease and Tauopathies.CNS & neurological disorders drug targets · 2024Review
- Article
- Rasd2 Mediates Acute Fasting-Induced Antidepressant-Like Effects via Dopamine D2 Receptor Activation in Ovariectomized Mice.The international journal of neuropsychopharmacology · 2023Article
- Rhes protein transits from neuron to neuron and facilitates mutant huntingtin spreading in the brain.Science advances · 2022Article
- Regulation of GTPase function by autophosphorylation.Molecular cell · 2022Article
- Striatal Induction and Spread of the Huntington's Disease Protein: A Novel Rhes Route.Journal of Huntington's disease · 2022Review
- 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
- Biophysical and Structural Characterization of Novel RAS-Binding Domains (RBDs) of PI3Kα and PI3Kγ.Journal of molecular biology · 2021Article
- Rhes Tunnels: A Radical New Way of Communication in the Brain's Striatum?BioEssays : news and reviews in molecular, cellular and developmental biology · 2020Review
- Exaggerated mitophagy: a weapon of striatal destruction in the brain?Biochemical Society transactions · 2020Review
- Rhes, a striatal-enriched protein, promotes mitophagy via Nix.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The striatal-enriched protein Rhes is a critical modulator of cocaine-induced molecular and behavioral responses.Scientific reports · 2019Article
- The Emerging Roles of Ferroptosis in Huntington's Disease.Neuromolecular medicine · 2019Review
- A farnesyltransferase inhibitor activates lysosomes and reduces tau pathology in mice with tauopathy.Science translational medicine · 2019Article
- Transport, Metabolism, and Function of Thyroid Hormones in the Developing Mammalian Brain.Frontiers in endocrinology · 2019Review
- MicroRNA-101 inhibits the expression of Rhes, a striatal-enriched small G-protein, at the post-transcriptional level in vitro.BMC research notes · 2018Article
- Rhes Counteracts Dopamine Neuron Degeneration and Neuroinflammation Depending on Gender and Age.Frontiers in aging neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ras homolog enriched in striatum, Rhes, is the product of a thyroid hormone-regulated gene during brain development. Rhes and the dexamethasone-induced Dexras1 define a novel distinct subfamily of proteins within the Ras family, characterized by an extended variable domain in the carboxyl terminal region. We have carried this study because there is a complete lack of knowledge on Rhes signaling. We show that in PC12 cells, Rhes is targeted to the plasma membrane by farnesylation. We demonstrate that about 30% of the native Rhes protein is bound to GTP and this proportion is unaltered by typical Ras family nucleotide exchange factors. However, Rhes is not transforming in murine fibroblasts. We have also examined the role of Rhes in cell signaling. Rhes does not stimulate the ERK pathway. By contrast, it binds to and activates PI3K. On the other hand, we demonstrate that Rhes impairs the activation of the cAMP/PKA pathway by thyroid-stimulating hormone, and by an activated beta2 adrenergic receptor by a mechanism that suggests uncoupling of the receptor to its cognate heterotrimeric complex. Overall, our results provide the initial insights into the role in signal transduction of this novel Ras family member.
Indexed as
Identifiers
What OpenQuestion holds
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.