ArticleCell stress & chaperones2001
Heat shock factor 1-mediated thermotolerance prevents cell death and results in G2/M cell cycle arrest.
Article in Cell stress & chaperones, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 53 citations in OpenAlex.
- A guide to heat shock factors as multifunctional transcriptional regulators.The FEBS journal · 2025Review
- Heat Shock Factor 1 Inhibition: A Novel Anti-Cancer Strategy with Promise for Precision Oncology.Cancers · 2023Review
- Targeting HSF1 for cancer treatment: mechanisms and inhibitor development.Theranostics · 2023Review
- Review
- Stress-induced transcriptional memory accelerates promoter-proximal pause release and decelerates termination over mitotic divisions.Molecular cell · 2021Article
- HSF1: Primary Factor in Molecular Chaperone Expression and a Major Contributor to Cancer Morbidity.Cells · 2020Review
- Interplay between HSF1 and p53 signaling pathways in cancer initiation and progression: non-oncogene and oncogene addiction.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- A Bioinformatic Approach for the Identification of Molecular Determinants of Resistance/Sensitivity to Cancer Thermotherapy.Oxidative medicine and cellular longevity · 2019Article
- Oxidative stress-induced DNA damage of mouse zygotes triggers G2/M checkpoint and phosphorylates Cdc25 and Cdc2.Cell stress & chaperones · 2016Article
- Forkhead box M1 is regulated by heat shock factor 1 and promotes glioma cells survival under heat shock stress.The Journal of biological chemistry · 2013Article
- Functional HSF1 requires aromatic-participant interactions in protecting mouse embryonic fibroblasts against apoptosis via G2 cell cycle arrest.Molecules and cells · 2012Article
- Induction of heat shock proteins by hyperthermia and noise overstimulation in hsf1 -/- mice.Journal of the Association for Research in Otolaryngology : JARO · 2012Article
- Hyperthermia-associated carboplatin resistance: differential role of p53, HSF1 and Hsp70 in hepatoma cells.Cancer science · 2010Article
- Heat shock factor-1 modulates p53 activity in the transcriptional response to DNA damage.Nucleic acids research · 2009Article
- Enhanced tolerance to chilling stress in OsMYB3R-2 transgenic rice is mediated by alteration in cell cycle and ectopic expression of stress genes.Plant physiology · 2009Article
- Clustering of genes into regulons using integrated modeling-COGRIM.Genome biology · 2007Article
- Genomic instability and enhanced radiosensitivity in Hsp70.1- and Hsp70.3-deficient mice.Molecular and cellular biology · 2004Article
- Identifying cooperativity among transcription factors controlling the cell cycle in yeast.Nucleic acids research · 2003Article
- Localized recruitment of a chromatin-remodeling activity by an activator in vivo drives transcriptional elongation.Genes & development · 2003Article
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
Mammalian cells respond to environmental stress by activating heat shock transcription factors (eg, Hsf1) that regulate increased synthesis of heat shock proteins (Hsps). Hsps prevent the disruption of normal cellular mitosis, meiosis, or differentiation by environmental stressors. To further characterize this stress response, transformed wild-type Hsf1+/+ and mutant Hsf1-/- mouse embryonic fibroblasts (MEFs) were exposed to (1) lethal heat (45 degrees C, 60 minutes), (2) conditioning heat (43 degrees C, 30 minutes), or (3) conditioning followed by lethal heat. Western blot analysis demonstrated that only Hsf1+/+ MEFs expressed inducible Hsp70s and Hsp25 following conditioning or conditioning and lethal heat. Exposure of either Hsf1+/+ or Hsf1-/- MEFs to lethal heat resulted in cell death. However, if conditioning heat was applied 6 hours before lethal heat, more than 85% of Hsf1+/+ MEFs survived, and cells in G2/M transiently increased 3-fold. In contrast, conditioned Hsf1-/- MEFs neither survived lethal heat nor exhibited this G2/M accumulation. Coinfection with adenoviral Hsp70 and Hsp25 constructs did not fully recreate thermotolerance in either Hsf1+/+ or Hsf1-/- MEFs, indicating other Hsf1-mediated gene expression is required for complete thermotolerance. These results demonstrate the necessity of Hsf1-mediated gene expression for thermotolerance and the involvement of cell cycle regulation, particularly the G2/M transition, in this thermotolerant response.
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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.