ArticleThe Journal of biological chemistry2012
Prothymosin-α interacts with mutant huntingtin and suppresses its cytotoxicity in cell culture.
Article in The Journal of biological chemistry, 2012. 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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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Heat Shock-Induced Extracellular Vesicles Derived from Neural Stem Cells Confer Marked Neuroprotection Against Oxidative Stress and Amyloid-β-Caused Neurotoxicity.Molecular neurobiology · 2022Article
- The cytoprotective role of GM1 ganglioside in Huntington disease cells.Molecular biology reports · 2022Article
- Mutant Huntingtin Protein Interaction Map Implicates Dysregulation of Multiple Cellular Pathways in Neurodegeneration of Huntington's Disease.Journal of Huntington's disease · 2022Article
- Attenuation of Ischemic Stroke-Caused Brain Injury by a Monoamine Oxidase Inhibitor Involves Improved Proteostasis and Reduced Neuroinflammation.Molecular neurobiology · 2020Article
- FOXOs modulate proteasome activity in human-induced pluripotent stem cells of Huntington's disease and their derived neural cells.Human molecular genetics · 2017Article
- Enhanced Proteostasis in Post-ischemic Stroke Mouse Brains by Ubiquilin-1 Promotes Functional Recovery.Cellular and molecular neurobiology · 2017Article
- Heterologous expression, purification and characterization of three novel esterases secreted by the lignocellulolytic fungus Penicillium purpurogenum when grown on sugar beet pulp.Carbohydrate research · 2017Article
- USP14 inhibitor attenuates cerebral ischemia/reperfusion-induced neuronal injury in mice.Journal of neurochemistry · 2017Article
- Properties of Two Novel Esterases Identified from Culture Supernatant ofInsights in enzyme research · 2016Article
- Shotgun Proteomics Analysis of Estrogen Effects in the Uterus Using Two-Dimensional Liquid Chromatography and Tandem Mass Spectrometry.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Sulforaphane enhances proteasomal and autophagic activities in mice and is a potential therapeutic reagent for Huntington's disease.Journal of neurochemistry · 2014Article
- The proteasome function reporter GFPu accumulates in young brains of the APPswe/PS1dE9 Alzheimer's disease mouse model.Cellular and molecular neurobiology · 2014Article
- Ubiquilin-1 protects cells from oxidative stress and ischemic stroke caused tissue injury in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Article
- Prefoldin protects neuronal cells from polyglutamine toxicity by preventing aggregation formation.The Journal of biological chemistry · 2013Article
- Transient focal cerebral ischemia upregulates immunoproteasomal subunits.Cellular and molecular neurobiology · 2012Article
- Mass spectrometric identification of novel posttranslational modification sites in Huntingtin.Proteomics · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Huntington disease (HD), a fatal neurodegenerative disorder, is caused by a lengthening of the polyglutamine tract in the huntingtin (Htt) protein. Despite considerable effort, thus far there is no cure or treatment available for the disorder. Using the approach of tandem affinity purification we recently discovered that prothymosin-α (ProTα), a small highly acidic protein, interacts with mutant Htt (mHtt). This was confirmed by co-immunoprecipitation and a glutathione S-transferase (GST) pull-down assay. Overexpression of ProTα remarkably reduced mHtt-induced cytotoxicity in both non-neuronal and neuronal cell models expressing N-terminal mHtt fragments, whereas knockdown of ProTα expression in the cells enhanced mHtt-caused cell death. Deletion of the central acidic domain of ProTα abolished not only its interaction with mHtt but also its protective effect on mHtt-caused cytotoxicity. Additionally, overexpression of ProTα inhibited caspase-3 activation but enhanced aggregation of mHtt. Furthermore, when added to cultured cells expressing mHtt, the purified recombinant ProTα protein not only entered the cells but it also significantly suppressed the mHtt-caused cytotoxicity. Taken together, these data suggest that ProTα might be a novel therapeutic target for treating HD and other polyglutamine expansion disorders.
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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.