ArticleThe Journal of cell biology2014
Expression of HSF2 decreases in mitosis to enable stress-inducible transcription and cell survival.
Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- The Function of Heat Shock Transcription Factors in Sex Differentiation inAnimals : an open access journal from MDPI · 2025Article
- Heat shock factor 2 regulates oncogenic gamma-herpesvirus gene expression by remodeling the chromatin at the ORF50 and BZLF1 promoter.PLoS pathogens · 2025Article
- Nuclear architecture and the structural basis of mitotic memory.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- DNAJC24 is a potential therapeutic target in hepatocellular carcinoma through affecting ammonia metabolism.Cell death & disease · 2022Article
- Heat Shock Proteins and HSF1 in Cancer.Frontiers in oncology · 2022Review
- Heat shock factor 1 suppression induces spindle abnormalities and sensitizes cells to antimitotic drugs.Cell division · 2021Article
- Stress-induced transcriptional memory accelerates promoter-proximal pause release and decelerates termination over mitotic divisions.Molecular cell · 2021Article
- Modulating the Heat Stress Response to Improve Hyperthermia-Based Anticancer Treatments.Cancers · 2021Review
- The proteostasis guardian HSF1 directs the transcription of its paralog and interactor HSF2 during proteasome dysfunction.Cellular and molecular life sciences : CMLS · 2021Article
- Heat shock factor 5 correlated with immune infiltration serves as a prognostic biomarker in lung adenocarcinoma.International journal of medical sciences · 2021Article
- Tailoring of Proteostasis Networks with Heat Shock Factors.Cold Spring Harbor perspectives in biology · 2019Review
- Molecular mechanisms driving transcriptional stress responses.Nature reviews. Genetics · 2018Review
- Regulation of heat shock transcription factors and their roles in physiology and disease.Nature reviews. Molecular cell biology · 2018Review
- Chaperone co-inducer BGP-15 inhibits histone deacetylases and enhances the heat shock response through increased chromatin accessibility.Cell stress & chaperones · 2017Article
- Transcriptional response to stress is pre-wired by promoter and enhancer architecture.Nature communications · 2017Article
- Metabolic control of the proteotoxic stress response: implications in diabetes mellitus and neurodegenerative disorders.Cellular and molecular life sciences : CMLS · 2016Review
- Article
- Mammalian Heat Shock Response and Mechanisms Underlying Its Genome-wide Transcriptional Regulation.Molecular cell · 2016Article
- Structures of HSF2 reveal mechanisms for differential regulation of human heat-shock factors.Nature structural & molecular biology · 2016Article
- The Role of the Membrane-Initiated Heat Shock Response in Cancer.Frontiers in molecular biosciences · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unless mitigated, external and physiological stresses are detrimental for cells, especially in mitosis, resulting in chromosomal missegregation, aneuploidy, or apoptosis. Heat shock proteins (Hsps) maintain protein homeostasis and promote cell survival. Hsps are transcriptionally regulated by heat shock factors (HSFs). Of these, HSF1 is the master regulator and HSF2 modulates Hsp expression by interacting with HSF1. Due to global inhibition of transcription in mitosis, including HSF1-mediated expression of Hsps, mitotic cells are highly vulnerable to stress. Here, we show that cells can counteract transcriptional silencing and protect themselves against proteotoxicity in mitosis. We found that the condensed chromatin of HSF2-deficient cells is accessible for HSF1 and RNA polymerase II, allowing stress-inducible Hsp expression. Consequently, HSF2-deficient cells exposed to acute stress display diminished mitotic errors and have a survival advantage. We also show that HSF2 expression declines during mitosis in several but not all human cell lines, which corresponds to the Hsp70 induction and protection against stress-induced mitotic abnormalities and apoptosis.
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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.