ArticleProceedings of the National Academy of Sciences of the United States of America2008
Heat shock factor 1 regulates lifespan as distinct from disease onset in prion disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 67 citations in OpenAlex.
- Trial
- 1-L Transcription in Prion Diseases.International journal of molecular sciences · 2024Article
- Deactivation of the Unfolded Protein Response Aggravated Renal AA Amyloidosis in HSF1 Deficiency Mice.Molecular and cellular biology · 2024Article
- Clearance of variant Creutzfeldt-Jakob disease prions in vivo by the Hsp70 disaggregase system.Brain : a journal of neurology · 2022Article
- Proteostasis unbalance in prion diseases: Mechanisms of neurodegeneration and therapeutic targets.Frontiers in neuroscience · 2022Review
- HSB-1/HSF-1 pathway modulates histone H4 in mitochondria to control mtDNA transcription and longevity.Science advances · 2020Article
- Feedback regulation of heat shock factor 1 (Hsf1) activity by Hsp70-mediated trimer unzipping and dissociation from DNA.The EMBO journal · 2020Article
- Molecular Chaperones: A Double-Edged Sword in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Review
- Prion disease is accelerated in mice lacking stress-induced heat shock protein 70 (HSP70).The Journal of biological chemistry · 2019Article
- Impaired neural stem cell expansion and hypersensitivity to epileptic seizures in mice lacking the EGFR in the brain.The FEBS journal · 2018Article
- Prions, prionoids and protein misfolding disorders.Nature reviews. Genetics · 2018Review
- Acetylation-induced TDP-43 pathology is suppressed by an HSF1-dependent chaperone program.Nature communications · 2017Article
- Determinants of rodent longevity in the chaperone-protein degradation network.Cell stress & chaperones · 2016Article
- Uncoupling Stress-Inducible Phosphorylation of Heat Shock Factor 1 from Its Activation.Molecular and cellular biology · 2015Article
- The unpredictability of prolonged activation of stress response pathways.The Journal of cell biology · 2015Article
- Modulation of the maladaptive stress response to manage diseases of protein folding.PLoS biology · 2014Article
- HSF1 protects neurons through a novel trimerization- and HSP-independent mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Combined pharmacological induction of Hsp70 suppresses prion protein neurotoxicity in Drosophila.PloS one · 2014Article
- Heat shock factor 1 over-expression protects against exposure of hydrophobic residues on mutant SOD1 and early mortality in a mouse model of amyotrophic lateral sclerosis.Molecular neurodegeneration · 2013Article
- Heat shock transcription factor 1 is activated as a consequence of lymphocyte activation and regulates a major proteostasis network in T cells critical for cell division during stress.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Prion diseases are fatal, transmissible, neurodegenerative diseases caused by the misfolding of the prion protein (PrP). At present, the molecular pathways underlying prion-mediated neurotoxicity are largely unknown. We hypothesized that the transcriptional regulator of the stress response, heat shock factor 1 (HSF1), would play an important role in prion disease. Uninoculated HSF1 knockout (KO) mice used in our study do not show signs of neurodegeneration as assessed by survival, motor performance, or histopathology. When inoculated with Rocky Mountain Laboratory (RML) prions HSF1 KO mice had a dramatically shortened lifespan, succumbing to disease approximately 20% faster than controls. Surprisingly, both the onset of home-cage behavioral symptoms and pathological alterations occurred at a similar time in HSF1 KO and control mice. The accumulation of proteinase K (PK)-resistant PrP also occurred with similar kinetics and prion infectivity accrued at an equal or slower rate. Thus, HSF1 provides an important protective function that is specifically manifest after the onset of behavioral symptoms of prion disease.
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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.