ArticleMolecular and cellular biology2004
Rhes is involved in striatal function.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 70 citations in OpenAlex.
- Membrane-associated Rhes-Slc4a7 complex orchestrates tunneling nanotube formation and mutant Huntingtin spread.Science advances · 2026Article
- 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
- Rhes depletion promotes striatal accumulation and aggregation of mutant huntingtin in a presymptomatic HD mouse model.Frontiers in aging neuroscience · 2023Article
- Huntington's disease phenotypes are improved via mTORC1 modulation by small molecule therapy.PloS one · 2022Article
- Article
- Loss of Hap1 selectively promotes striatal degeneration in Huntington disease mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Age effect on thyroid hormone brain response in male mice.Endocrine · 2019Article
- A farnesyltransferase inhibitor activates lysosomes and reduces tau pathology in mice with tauopathy.Science translational medicine · 2019Article
- The Ras Superfamily of Small GTPases in Non-neoplastic Cerebral Diseases.Frontiers in molecular neuroscience · 2019Review
- Transport, Metabolism, and Function of Thyroid Hormones in the Developing Mammalian Brain.Frontiers in endocrinology · 2019Review
- RasGRP1 promotes amphetamine-induced motor behavior through a Rhes interaction network ("Rhesactome") in the striatum.Science signaling · 2016Article
- Rasd2 Modulates Prefronto-Striatal Phenotypes in Humans and 'Schizophrenia-Like Behaviors' in Mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Rhes influences striatal cAMP/PKA-dependent signaling and synaptic plasticity in a gender-sensitive fashion.Scientific reports · 2015Article
- Activators of G protein signaling in the kidney.The Journal of pharmacology and experimental therapeutics · 2015Review
- Localization and expression profile of Group I and II Activators of G-protein Signaling in the kidney.Journal of molecular histology · 2015Article
- Reinstating aberrant mTORC1 activity in Huntington's disease mice improves disease phenotypes.Neuron · 2015Article
- Activators of G protein signaling exhibit broad functionality and define a distinct core signaling triad.Molecular pharmacology · 2014Review
- Preclinical and clinical investigations of mood stabilizers for Huntington's disease: what have we learned?International journal of biological sciences · 2014Review
- Small G Proteins Dexras1 and RHES and Their Role in Pathophysiological Processes.International journal of cell biology · 2014Review
- Rhes suppression enhances disease phenotypes in Huntington's disease mice.Journal of Huntington's disease · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development and the function of central nervous system depend on thyroid hormones. In humans, the lack of thyroid hormones causes cretinism, a syndrome of severe mental deficiency. It is assumed that thyroid hormones affect the normal development and function of the brain by activating or suppressing target gene expression because several genes expressed in the brain have been shown to be under thyroid hormone control. Among these, the Rhes gene, encoding a small GTP-binding protein, is predominantly expressed in the striatal region of the brain. To clarify the role of Rhes in vivo, we disrupted the Rhes gene by homologous recombination in embryonic stem cells and generated mice homozygous for the Rhes null mutation (Rhes(-/-)). Rhes(-/-) mice were viable but weighed less than wild-type mice. Furthermore, they showed behavioral abnormalities, displaying a gender-dependent increase in anxiety levels and a clear motor coordination deficit but no learning or memory impairment. These results suggest that Rhes disruption affects selected behavioral competencies.
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.