An additional long-term mechanism of NF-κB regulation after cytokine treatment in a human hepatoma cell line.
The eukaryotic transcription factor nuclear factor-κB (NF-κB) is mainly involved in the regulation of immune response and inflammation. A prolonged activation of NF-κB has been reported in context with chronic diseases. What leads to a prolongation of NF-κB activity is not well understood. Here, an increase in total intracellular NF-κB protein and mRNA levels as well as a temporary colocalization of NF-κB with proteasomes in human hepatocytes after treatment with TNF-α or IL-1β is reported. This indicates that beside an instantaneous activation of NF-κB and partly autoregulated inactivation by breakdown and synthesis of the inhibitors of NF-κB (IκBs), there are also mechanisms for a long-term regulation by de novo-synthesis and degradation of NF-κB protein.
Kohlhof
Patricia
P
Institute of Anatomy and Cell Biology II, University of Heidelberg, Germany. P.Kohlhof@klinikum-stuttgart.de
D015152:Blotting, Northern; D015153:Blotting, Western; D006528:Carcinoma, Hepatocellular / Q000378:metabolism*; D045744:Cell Line, Tumor; D005455:Fluorescent Antibody Technique; D005786:Gene Expression Regulation / Q000502:physiology*; D006801:Humans; D007150:Immunohistochemistry; D053583:Interleukin-1beta / Q000378:metabolism*; D008113:Liver Neoplasms / Q000378:metabolism*; D046529:Microscopy, Electron, Transmission; D016328:NF-kappa B / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D053583:Interleukin-1beta; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha