ArticleMetabolic brain disease2019
Genistein induces degradation of mutant huntingtin in fibroblasts from Huntington's disease patients.
Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.
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Who cites it
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.
- A systematic review of natural products targeting Nrf2-Keap1-ARE pathway and their influence on neurodegenerative disorders.Inflammopharmacology · 2025Pooled it
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- [Application ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- AI-Enhanced Transcriptomic Discovery of Druggable Targets and Repurposed Therapies for Huntington's Disease.Brain sciences · 2025Review
- Cardiovascular Risk Factors, Alzheimer's Disease, and the MIND Diet: A Narrative Review from Molecular Mechanisms to Clinical Outcomes.Nutrients · 2025Review
- Isothiocyanates induce autophagy and inhibit protein synthesis in primary cells via modulation of AMPK-mTORC1-S6K1 signaling pathway, and protect against mutant huntingtin aggregation.European journal of nutrition · 2024Article
- The Role of Gene Expression Dysregulation in the Pathogenesis of Mucopolysaccharidosis: A Comparative Analysis of Shared and Specific Molecular Markers in Neuronopathic and Non-Neuronopathic Types of the Disease.International journal of molecular sciences · 2024Article
- Effectiveness of Flavonoid-Rich Diet in Alleviating Symptoms of Neurodegenerative Diseases.Foods (Basel, Switzerland) · 2024Review
- Correction of symptoms of Huntington disease by genistein through FOXO3-mediated autophagy stimulation.Autophagy · 2024Article
- Tubulin Cytoskeleton in Neurodegenerative Diseases-not Only Primary Tubulinopathies.Cellular and molecular neurobiology · 2023Review
- A Progressive Loss of phosphoSer138-Profilin Aligns with Symptomatic Course in the R6/2 Mouse Model of Huntington's Disease: Possible Sex-Dependent Signaling.Cellular and molecular neurobiology · 2022Article
- Genistein: A Potential Natural Lead Molecule for New Drug Design and Development for Treating Memory Impairment.Molecules (Basel, Switzerland) · 2022Review
- Zebrafish an experimental model of Huntington's disease: molecular aspects, therapeutic targets and current challenges.Molecular biology reports · 2021Review
- Transcriptomic Changes Related to Cellular Processes with Particular Emphasis on Cell Activation in Lysosomal Storage Diseases from the Group of Mucopolysaccharidoses.International journal of molecular sciences · 2020Article
- Genetic Base of Behavioral Disorders in Mucopolysaccharidoses: Transcriptomic Studies.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the HTT gene, consisting of expansion of CAG triplets, cause the Huntington's disease (HD), one of the major neurodegenerative disorders. Formation of aggregates of mutant huntingtin (mHTT, the product of the mutant HTT gene) leads to cellular dysfunctions, and subsequent neurodegeneration which manifest clinically as motor abnormalities and cognitive deficits. We recently used immortalized HEK-293 cells expressing the 1st exon of the mutant HTT gene as a cellular model of HD, and showed that the stimulation of autophagy by genistein corrected the mutant phenotype. However, effects of genistein on HD patient-derived cells remained unknown. In this report, we demonstrated that genistein also instigated degradation of mHTT in fibroblasts derived from HD patients. This was assessed as a significant decrease in the levels of HTT in HD fibroblasts measured by Western-blotting, and the disappearance of intracellular mHTT aggregates in cells observed by fluorescent microscopy. Fibroblasts derived from control persons were not affected by genistein treatment. These results indicate that genistein can improve HD phenotype in patient-derived cells, and substantiates the need for further studies of this isoflavone as a potential therapeutic agent.
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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.