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.
- 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.