Inhibition of NF-κB cellular function via specific targeting of the IκB-ubiquitin ligase

Activation of the transcription factor NF‐κB is a paradigm for signal transduction through the ubiquitin–proteasome pathway: ubiquitin‐dependent degradation of the transcriptional inhibitor IκB in response to cell stimulation. A major issue in this context is the nature of the recognition signal and...

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Veröffentlicht in:	The EMBO journal 1997-11, Vol.16 (21), p.6486-6494
Hauptverfasser:	Yaron, Avraham, Gonen, Hedva, Alkalay, Irit, Hatzubai, Ada, Jung, Steffen, Beyth, Shaul, Mercurio, Frank, Manning, Anthony M., Ciechanover, Aaron, Ben-Neriah, Yinon
Format:	Artikel
Sprache:	eng
Schlagworte:	Amino Acid Sequence Biological Transport Cell Nucleus - metabolism Cells, Cultured Cysteine Endopeptidases - metabolism Cytoplasm - metabolism degradation E-Selectin - biosynthesis E-Selectin - genetics Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism HeLa Cells - drug effects HeLa Cells - metabolism Humans IκB phosphorylation Jurkat Cells - drug effects Jurkat Cells - metabolism Ligases - antagonists & inhibitors Ligases - physiology Molecular Sequence Data Multienzyme Complexes - metabolism NF-kappa B - antagonists & inhibitors NF-κB Peptide Fragments - pharmacology Phosphorylation - drug effects Proteasome Endopeptidase Complex Protein Processing, Post-Translational - drug effects Proto-Oncogene Proteins - metabolism Signal Transduction - drug effects Signal Transduction - physiology Transcription Factor RelB Transcription Factors Transcription, Genetic - drug effects ubiquitin ubiquitin ligase motif Ubiquitin-Protein Ligases Ubiquitins - metabolism Umbilical Veins
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