ArticleCell stress & chaperones2013
A delayed antioxidant response in heat-stressed cells expressing a non-DNA binding HSF1 mutant.
Article in Cell stress & chaperones, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Coping with harsh heat environments: molecular adaptation of metabolic depression in the intertidal snail Echinolittorina radiata.Cell stress & chaperones · 2023Article
- Interfering with the expression of EEF1D gene enhances the sensitivity of ovarian cancer cells to cisplatin.BMC cancer · 2022Article
- Hsp70 in Redox Homeostasis.Cells · 2022Review
- The role of EEF1D in disease pathogenesis: a narrative review.Annals of translational medicine · 2021Review
- Beyond Heat Stress: Intestinal Integrity Disruption and Mechanism-Based Intervention Strategies.Nutrients · 2020Review
- Remote Control of Mammalian Cells with Heat-Triggered Gene Switches and Photothermal Pulse Trains.ACS synthetic biology · 2018Article
- NK cells of the oldest seniors represent constant and resistant to stimulation high expression of cellular protective proteins SIRT1 and HSP70.Immunity & ageing : I & A · 2018Article
- Physical activity profile of 2014 FIFA World Cup players, with regard to different ranges of air temperature and relative humidity.International journal of biometeorology · 2017Article
- Cross talk between cytokine and hyperthermia-induced pathways: identification of different subsets of NF-κB-dependent genes regulated by TNFα and heat shock.Molecular genetics and genomics : MGG · 2015Article
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5 authors.
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Abstract
To assess the consequences of inactivation of heat shock factor 1 (HSF1) during aging, we analyzed the effect of HSF1 K80Q, a mutant unable to bind DNA, and of dnHSF1, a mutant lacking the activation domain, on the transcriptome of cells 6 and 24 h after heat shock. The primary response to heat shock (6 h recovery), of which 30 % was HSF1-dependent, had decayed 24 h after heat shock in control cells but was extended in HSF1 K80Q and dnHSF1 cells. Comparison with literature data showed that even the HSF1 dependent primary stress response is largely cell specific. HSF1 K80Q, but not HSF1 siRNA-treated, cells showed a delayed stress response: an increase in transcript levels of HSF1 target genes 24 h after heat stress. Knockdown of NRF2, but not of ATF4, c-Fos or FosB, inhibited this delayed stress response. EEF1D_L siRNA inhibited both the delayed and the extended primary stress responses, but had off target effects. In control cells an antioxidant response (ARE binding, HMOX1 mRNA levels) was detected 6 h after heat shock; in HSF1 K80Q cells this response was delayed to 24 h and the ARE complex had a different mobility. Inactivation of HSF1 thus affects the timing and nature of the antioxidant response and NRF2 can activate at least some HSF1 target genes in the absence of HSF1 activity.
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