ReviewJournal of molecular neuroscience : MN2004
Role of heat shock proteins during polyglutamine neurodegeneration: mechanisms and hypothesis.
Review in Journal of molecular neuroscience : MN, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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Who cites it
32 citing papers in PubMed.
- Disrupted Transcriptional Networks in Mammalian Cells Stably Over-Expressing Pathogenic Atrophin-1.Journal of neuroscience research · 2025Article
- Disrupted Transcriptional Networks by Mutant Atrophin-1 in a Cell Culture Model of Dentatorubral-Pallidoluysian Atrophy.bioRxiv : the preprint server for biology · 2025Article
- Reviewing the Structure-Function Paradigm in Polyglutamine Disorders: A Synergistic Perspective on Theoretical and Experimental Approaches.International journal of molecular sciences · 2024Review
- Contribution of Extracellular Vesicles and Molecular Chaperones in Age-Related Neurodegenerative Disorders of the CNS.International journal of molecular sciences · 2023Review
- Heat shock proteins: Biological functions, pathological roles, and therapeutic opportunities.MedComm · 2022Review
- Review
- Hsc70-4 aggravates PolyQ-mediated neurodegeneration by modulating NF-κB mediated immune response inFrontiers in molecular neuroscience · 2022Article
- Exploring the Potential of Small Molecule-Based Therapeutic Approaches for Targeting Trinucleotide Repeat Disorders.Molecular neurobiology · 2020Review
- Pharmacological induction of heat shock proteins ameliorates toxicity of mutant PKCγ in spinocerebellar ataxia type 14.The Journal of biological chemistry · 2018Article
- Mutant Huntingtin Inhibits αB-Crystallin Expression and Impairs Exosome Secretion from Astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Review
- Current understanding of the molecular mechanisms in Parkinson's disease: Targets for potential treatments.Translational neurodegeneration · 2017Review
- Protein Quality Control by Molecular Chaperones in Neurodegeneration.Frontiers in neuroscience · 2017Review
- Polyglutamine androgen receptor-mediated neuromuscular disease.Cellular and molecular life sciences : CMLS · 2016Review
- Diverging Novobiocin Anti-Cancer Activity from Neuroprotective Activity through Modification of the Amide Tail.ACS medicinal chemistry letters · 2016Article
- αB-Crystallin overexpression in astrocytes modulates the phenotype of the BACHD mouse model of Huntington's disease.Human molecular genetics · 2016Article
- Geldanamycin attenuates 3‑nitropropionic acid‑induced apoptosis and JNK activation through the expression of HSP 70 in striatal cells.International journal of molecular medicine · 2014Article
- Molecular chaperone dysfunction in neurodegenerative diseases and effects of curcumin.BioMed research international · 2014Review
- Association of heat-shock proteins in various neurodegenerative disorders: is it a master key to open the therapeutic door?Molecular and cellular biochemistry · 2014Review
- Heat shock transcription factor-1 suppresses apoptotic cell death and ROS generation in 3-nitropropionic acid-stimulated striatal cells.Molecular and cellular biochemistry · 2013Article
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
A common feature of many neurodegenerative diseases, including Alzheimer's and Parkinsons's disease, the prion disorders, and the CAG repeat polyglutamine (polyQ) diseases, is the occurrence of protein aggregates within or outside of nerve cells. Molecular chaperones such as heat shock proteins (HSPs) have been proposed to play a critical role in preventing the accumulation of misfolded proteins that lead to the deposition of aggregates during pathology. This article focuses on the role of HSPs during polyQ pathologies, which include Huntington's disease, spinal and bulbar muscular atrophy, dentatorubral and pallidoluysian atrophy, and several forms of spinocerebellar ataxia. Recently, unifying mechanisms that are involved during polyQ disease have emerged, such as abnormal transcription, impaired degradation systems, and interference of a polyQ expansion with neuronal survival and death-signaling pathways like the activation of caspases and kinases. This article reviews recent studies that point to the involvement of these mechanisms during polyQ pathology and discusses how HSPs can interfere with such processes by paying special attention to HSPs as modulators of survival and death-signaling pathways.
Indexed as
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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.