Ectopic expression of the striatal-enriched GTPase Rhes elicits cerebellar degeneration and an ataxia phenotype in Huntington's disease
Author:
Funder
Scripps startup funds
Publisher
Elsevier BV
Subject
Neurology
Reference84 articles.
1. Creatine increase survival and delays motor symptoms in a transgenic animal model of Huntington's disease;Andreassen;Neurobiol. Dis.,2001
2. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death;Arrasate;Nature,2004
3. Attenuation of Rhes activity significantly delays the appearance of behavioral symptoms in a mouse model of Huntington's disease;Baiamonte;PLoS One,2013
4. Striatum specific protein, Rhes regulates AKT pathway;Bang;Neurosci. Lett.,2012
5. Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity;Caillard;Proc. Natl. Acad. Sci. U. S. A.,2000
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1. 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;2024-04-08
2. SUMO modifies GβL and mediates mTOR signaling;Journal of Biological Chemistry;2024-04
3. Curbing Rhes Actions: Mechanism-based Molecular Target for Huntington’s Disease and Tauopathies;CNS & Neurological Disorders - Drug Targets;2024-01
4. Tunneling nanotubes;Mitochondrial Transplantation and Transfer;2024
5. Rhes depletion promotes striatal accumulation and aggregation of mutant huntingtin in a presymptomatic HD mouse model;Frontiers in Aging Neuroscience;2023-08-10
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