Heat Shock Transcription Factors

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  Subject Areas on Research

  • A cut above the other caspases. 
  • Abnormal degradation of the neuronal stress-protective transcription factor HSF1 in Huntington's disease. 
  • Akt phosphorylates and activates HSF-1 independent of heat shock, leading to Slug overexpression and epithelial-mesenchymal transition (EMT) of HER2-overexpressing breast cancer cells. 
  • Amplification and high-level expression of heat shock protein 90 marks aggressive phenotypes of human epidermal growth factor receptor 2 negative breast cancer. 
  • Glutamine attenuates lung injury and improves survival after sepsis: role of enhanced heat shock protein expression. 
  • Glutamine attenuation of cell death and inducible nitric oxide synthase expression following inflammatory cytokine-induced injury is dependent on heat shock factor-1 expression. 
  • Glutamine enhances heat shock protein 70 expression via increased hexosamine biosynthetic pathway activity. 
  • Glutamine's protection against cellular injury is dependent on heat shock factor-1. 
  • Glutamine-mediated attenuation of cellular metabolic dysfunction and cell death after injury is dependent on heat shock factor-1 expression. 
  • Glutamine-mediated dual regulation of heat shock transcription factor-1 activation and expression. 
  • HDAC6 controls major cell response pathways to cytotoxic accumulation of protein aggregates. 
  • Heat shock transcription factor 1 as a therapeutic target in neurodegenerative diseases. 
  • Oral glutamine enhances heat shock protein expression and improves survival following hyperthermia. 
  • Protective responses in the ischemic myocardium. 
  • Rewiring of Signaling Networks Modulating Thermotolerance in the Human Pathogen Cryptococcus neoformans. 
  • Targeting therapy-resistant prostate cancer via a direct inhibitor of the human heat shock transcription factor 1. 
  • The ABL2 kinase regulates an HSF1-dependent transcriptional program required for lung adenocarcinoma brain metastasis. 
  • The HSF-like transcription factor TBF1 is a major molecular switch for plant growth-to-defense transition. 
  • uORF-mediated translation allows engineered plant disease resistance without fitness costs.