Transcriptional control of the inflammatory response: a role for the CREB-binding protein (CBP).
The cellular pathophysiology of septic shock is characterized by the activation of genes in response to exposure of cells to bacterial lipopolysaccharide. Tumour necrosis factor-alpha (TNF-alpha) or endotoxin induce the activation of two major transcription factors, NF-kappa B (nuclear factor-kappaB) and AP-1 (activating protein-1), which in turn induce genes involved in chronic and acute inflammatory responses. The activity of both of them is regulated by phosphorylation and subsequent interaction with the coactivator protein CBP (CREB-binding protein). Thus, the limiting CBP may play an important role in the development of critical illness.
Matt
Theresia
T
Institute of Biochemistry, University of Innsbruck, Peter-Mayr-Strasse 1a, A-6020 Innsbruck. Theresia.Matt@uibk.ac.at
D050882:CREB-Binding Protein; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000503:physiopathology; D016328:NF-kappa B / Q000235:genetics; D009687:Nuclear Proteins / Q000378:metabolism*; D015534:Trans-Activators / Q000378:metabolism*; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D016328:NF-kappa B; D009687:Nuclear Proteins; D015534:Trans-Activators; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D050882:CREB-Binding Protein; C494363:CREBBP protein, human