ArticleNature communications2013
Heat shock factor-1 influences pathological lesion distribution of polyglutamine-induced neurodegeneration.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
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- NXP800 Activates the Unfolded Protein Response, Altering AR and E2F Function to Impact Castration-Resistant Prostate Cancer Growth.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Unfolded proteins and aggregates: The role of proteostasis in pseudoexfoliation pathology.Molecular vision · 2025Review
- RBM4-mediated intron excision of Hsf1 induces BDNF for cerebellar foliation.Communications biology · 2024Article
- Exercise attenuates polyglutamine-mediated neuromuscular degeneration in a mouse model of spinal and bulbar muscular atrophy.Journal of cachexia, sarcopenia and muscle · 2024Article
- Heat shock factor HSF1 regulates BDNF gene promoters upon acute stress in the hippocampus, together with pCREB.Journal of neurochemistry · 2023Article
- Closest horizons of Hsp70 engagement to manage neurodegeneration.Frontiers in molecular neuroscience · 2023Review
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Review
- Is pseudoexfoliation glaucoma a neurodegenerative disorder?Journal of biosciences · 2021Review
- The Role of Sex and Sex Hormones in Neurodegenerative Diseases.Endocrine reviews · 2020Review
- Src inhibition attenuates polyglutamine-mediated neuromuscular degeneration in spinal and bulbar muscular atrophy.Nature communications · 2019Article
- DNA methylation inhibitor attenuates polyglutamine-induced neurodegeneration by regulating Hes5.EMBO molecular medicine · 2019Article
- Tailoring of Proteostasis Networks with Heat Shock Factors.Cold Spring Harbor perspectives in biology · 2019Review
- Proteomic analysis identifies NPTX1 and HIP1R as potential targets of histone deacetylase-3-mediated neurodegeneration.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- Regulation of heat shock transcription factors and their roles in physiology and disease.Nature reviews. Molecular cell biology · 2018Review
- Ethanol Stimulates Locomotion via a GGenetics · 2017Article
- Acetylation-induced TDP-43 pathology is suppressed by an HSF1-dependent chaperone program.Nature communications · 2017Article
- Abnormal degradation of the neuronal stress-protective transcription factor HSF1 in Huntington's disease.Nature communications · 2017Article
- Protein misfolding in neurodegenerative diseases: implications and strategies.Translational neurodegeneration · 2017Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A crucial feature of adult-onset neurodegenerative diseases is accumulation of abnormal protein in specific brain regions, although the mechanism underlying this pathological selectivity remains unclear. Heat shock factor-1 is a transcriptional regulator of heat shock proteins, molecular chaperones that abrogate neurodegeneration by refolding and solubilizing pathogenic proteins. Here we show that heat shock factor-1 expression levels are associated with the accumulation of pathogenic androgen receptor in spinal and bulbar muscular atrophy, a polyglutamine-induced neurodegenerative disease. In heterozygous heat shock factor-1-knockout spinal and bulbar muscular atrophy mice, abnormal androgen receptor accumulates in the cerebral visual cortex, liver and pituitary, which are not affected in their genetically unmodified counterparts. The depletion of heat shock factor-1 also expands the distribution of pathogenic androgen receptor accumulation in other neuronal regions. Furthermore, lentiviral-mediated delivery of heat shock factor-1 into the brain of spinal and bulbar muscular atrophy mice topically suppresses the pathogenic androgen receptor accumulation and neuronal atrophy. These results suggest that heat shock factor-1 influences the pathological lesion selectivity in spinal and bulbar muscular atrophy.
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