Englerin A Stimulates PKCθ to Inhibit Insulin Signaling and to Simultaneously Activate HSF1: Pharmacologically Induced Synthetic Lethality
Copyright policy )Englerin A Stimulates PKCθ to Inhibit Insulin Signaling and to Simultaneously Activate HSF1: Pharmacologically Induced Synthetic Lethality
The natural product englerin A (EA) binds to and activates protein kinase C-θ (PKCθ). EA-dependent activation of PKCθ induces an insulin-resistant phenotype, limiting the access of tumor cells to glucose. At the same time, EA causes PKCθ-mediated phosphorylation and activation of the transcription factor heat shock factor 1, an inducer of glucose dependence. By promoting glucose addiction, while simultaneously starving cells of glucose, EA proves to be synthetically lethal to highly glycolytic tumors.
- National Institutes of Health United States
- National Institute of Health Pakistan
- N-Gene (Hungary) Hungary
- National Cancer Institute United States
- Center for Cancer Research United States
Cancer Research, Blotting, Western, Apoptosis, Mice, Sesquiterpenes, Guaiane, Heat Shock Transcription Factors, Animals, Humans, Immunoprecipitation, Insulin, Phosphorylation, Protein Kinase C, Cell Proliferation, Cell Biology, Kidney Neoplasms, DNA-Binding Proteins, Isoenzymes, Glucose, Oncology, Protein Kinase C-theta, Insulin Resistance, Signal Transduction, Transcription Factors
Cancer Research, Blotting, Western, Apoptosis, Mice, Sesquiterpenes, Guaiane, Heat Shock Transcription Factors, Animals, Humans, Immunoprecipitation, Insulin, Phosphorylation, Protein Kinase C, Cell Proliferation, Cell Biology, Kidney Neoplasms, DNA-Binding Proteins, Isoenzymes, Glucose, Oncology, Protein Kinase C-theta, Insulin Resistance, Signal Transduction, Transcription Factors
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).78 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 10% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 10% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 10%
Citations provided by BIP!Popularity provided by BIP!