Endoplasmic reticulum stress stimulates p53 expression through NF-κB activation

Induction of apoptosis by endoplasmic reticulum (ER) stress is implicated as the major factor in the development of multiple diseases. ER stress also appears to be a potentially useful major response to many chemotherapeutic drugs and environmental chemical compounds. A previous study has indicated...

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Veröffentlicht in:	PloS one 2012-07, Vol.7 (7), p.e39120
Hauptverfasser:	Lin, Wan-Chi, Chuang, Yu-Chi, Chang, Yung-Sheng, Lai, Ming-Derg, Teng, Yen-Ni, Su, Ih-Jen, Wang, Clay C C, Lee, Kuan-Han, Hung, Jui-Hsiang
Format:	Artikel
Sprache:	eng
Schlagworte:	Activation Apoptosis Biochemistry Biology Brefeldin A Brefeldin A - pharmacology Cancer Cell cycle Cell death Chemical compounds Chemotherapy Cycloheximide - pharmacology Dactinomycin - pharmacology Drugs Endoplasmic reticulum Endoplasmic Reticulum Stress Gene expression Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta HCT116 Cells HeLa Cells Humans Immunoglobulins Infectious diseases Kinases Localization MCF-7 Cells Medicine Molecular biology NF-kappa B - metabolism NF-κB protein Nuclear transport p53 Protein Pharmacy Phosphorylation Protein Processing, Post-Translational Protein Synthesis Inhibitors - pharmacology Proteins Regulators Rodents Science Serine Signal Transduction Signaling siRNA Stress Stresses Transcription, Genetic - drug effects Transcriptional Activation Translocation Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tunicamycin
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