Heat Shock Transcription Factors

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  Subject Areas on Research

  • A cut above the other caspases. 
  • A direct regulatory interaction between chaperonin TRiC and stress-responsive transcription factor HSF1. 
  • Abnormal degradation of the neuronal stress-protective transcription factor HSF1 in Huntington's disease. 
  • Activation signals regulate heat shock transcription factor 1 in human B lymphocytes. 
  • 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. 
  • Conservation of a stress response: human heat shock transcription factors functionally substitute for yeast HSF. 
  • Deciphering human heat shock transcription factor 1 regulation via post-translational modification in yeast. 
  • Genetic selection for constitutively trimerized human HSF1 mutants identifies a role for coiled-coil motifs in DNA binding. 
  • Genomic heat shock element sequences drive cooperative human heat shock factor 1 DNA binding and selectivity. 
  • 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 factor function and regulation in response to cellular stress, growth, and differentiation signals. 
  • Heat shock transcription factor 1 as a therapeutic target in neurodegenerative diseases. 
  • Heat shock transcription factor activates yeast metallothionein gene expression in response to heat and glucose starvation via distinct signalling pathways. 
  • Induction of cell stress through gene transfer of an engineered heat shock transcription factor enhances tumor immunogenicity. 
  • Inhibition of DNA binding by differential sumoylation of heat shock factors. 
  • Modulation of heat shock transcription factor 1 as a therapeutic target for small molecule intervention in neurodegenerative disease. 
  • Modulation of human heat shock factor trimerization by the linker domain. 
  • Oral glutamine enhances heat shock protein expression and improves survival following hyperthermia. 
  • Oxidative stress induced heat shock factor phosphorylation and HSF-dependent activation of yeast metallothionein gene transcription. 
  • Protective responses in the ischemic myocardium. 
  • Rational design and screening of peptide-based inhibitors of heat shock factor 1 (HSF1). 
  • Redox regulation of mammalian heat shock factor 1 is essential for Hsp gene activation and protection from stress. 
  • Regulation of heat shock transcription factors and their roles in physiology and disease. 
  • Rewiring of Signaling Networks Modulating Thermotolerance in the Human Pathogen Cryptococcus neoformans. 
  • Sensitization of tumor cells to fas killing through overexpression of heat-shock transcription factor 1. 
  • Structures of HSF2 reveal mechanisms for differential regulation of human heat-shock factors. 
  • The HSF-like transcription factor TBF1 is a major molecular switch for plant growth-to-defense transition. 
  • The loop domain of heat shock transcription factor 1 dictates DNA-binding specificity and responses to heat stress. 
  • The mammalian HSF4 gene generates both an activator and a repressor of heat shock genes by alternative splicing. 
  • Transcriptional activation of heat shock factor HSF1 probed by phosphopeptide analysis of factor 32P-labeled in vivo. 
  • uORF-mediated translation allows engineered plant disease resistance without fitness costs.