ArticlePloS one2011
Decreased striatal RGS2 expression is neuroprotective in Huntington's disease (HD) and exemplifies a compensatory aspect of HD-induced gene regulation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 63 citations in OpenAlex.
- Patient-derived induced pluripotent stem cells with a C9orf72 expansion as a model to study frontotemporal dementia pathologies.Molecular biology of the cell · 2025Article
- Curbing Rhes Actions: Mechanism-based Molecular Target for Huntington's Disease and Tauopathies.CNS & neurological disorders drug targets · 2024Review
- From Pathogenesis to Therapeutics: A Review of 150 Years of Huntington's Disease Research.International journal of molecular sciences · 2023Review
- Rhes depletion promotes striatal accumulation and aggregation of mutant huntingtin in a presymptomatic HD mouse model.Frontiers in aging neuroscience · 2023Article
- Striatal Induction and Spread of the Huntington's Disease Protein: A Novel Rhes Route.Journal of Huntington's disease · 2022Review
- Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease.Nature communications · 2021Article
- Reduced BloodFrontiers in aging neuroscience · 2021Article
- 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
- 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
- Longitudinal expression changes are weak correlates of disease progression in Huntington's disease.Brain communications · 2020Article
- Bioinformatics analysis of Ras homologue enriched in the striatum, a potential target for Huntington's disease therapy.International journal of molecular medicine · 2019Article
- Rhes, a striatal-enriched protein, promotes mitophagy via Nix.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Rhes travels from cell to cell and transports Huntington disease protein via TNT-like protrusion.The Journal of cell biology · 2019Article
- A farnesyltransferase inhibitor activates lysosomes and reduces tau pathology in mice with tauopathy.Science translational medicine · 2019Article
- The Emerging Role of microRNAs in Polyglutamine Diseases.Frontiers in molecular neuroscience · 2019Article
- Regulating the regulators: Epigenetic, transcriptional, and post-translational regulation of RGS proteins.Cellular signalling · 2018Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe molecular phenotype of Huntington's disease (HD) is known to comprise highly reproducible changes in gene expression involving striatal signaling genes. Here we test whether individual changes in striatal gene expression are capable of mitigating HD-related neurotoxicity. METHODOLOGY/PRINCIPAL
findingsWe used protein-encoding and shRNA-expressing lentiviral vectors to evaluate the effects of RGS2, RASD2, STEP and NNAT downregulation in HD. Of these four genes, only RGS2 and RASD2 modified mutant htt fragment toxicity in cultured rat primary striatal neurons. In both cases, disease modulation was in the opposite of the predicted direction: whereas decreased expression of RGS2 and RASD2 was associated with the HD condition, restoring expression enhanced degeneration of striatal cells. Conversely, silencing of RGS2 or RASD2 enhanced disease-related changes in gene expression and resulted in significant neuroprotection. These results indicate that RGS2 and RASD2 downregulation comprises a compensatory response that allows neurons to better tolerate huntingtin toxicity. Assessment of the possible mechanism of RGS2-mediated neuroprotection showed that RGS2 downregulation enhanced ERK activation. These results establish a novel link between the inhibition of RGS2 and neuroprotective modulation of ERK activity.
conclusionsOur findings both identify RGS2 downregulation as a novel compensatory response in HD neurons and suggest that RGS2 inhibition might be considered as an innovative target for neuroprotective drug development.
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.