The B1-agonist [des-Arg10]-kallidin activates transcription factor NF-kappaB and induces homologous upregulation of the bradykinin B1-receptor in cultured human lung fibroblasts

The bradykinin B1-receptor is strongly upregulated under chronic inflammatory conditions. However, the mechanism and reason are not known. Because a better understanding of the mechanism of the upregulation will help in understanding its potential importance in inflammation, we have studied the mole...

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Veröffentlicht in:	The Journal of clinical investigation 1998-05, Vol.101 (10), p.2080-2091
Hauptverfasser:	Schanstra, J P, Bataillé, E, Marin Castaño, M E, Barascud, Y, Hirtz, C, Pesquero, J B, Pecher, C, Gauthier, F, Girolami, J P, Bascands, J L
Format:	Artikel
Sprache:	eng
Schlagworte:	Amino Acid Sequence Cell Line Cholera Toxin - pharmacology DNA-Binding Proteins - metabolism Fibroblasts Humans Inflammation - physiopathology Interleukin-1 - pharmacology Kallidin - agonists Kallidin - analogs & derivatives Kallidin - pharmacology Lung - drug effects Molecular Sequence Data NF-kappa B - metabolism Proline - analogs & derivatives Proline - pharmacology Pyrrolidines - pharmacology Receptor, Bradykinin B1 Receptors, Bradykinin - metabolism RNA, Messenger - metabolism Thiocarbamates - pharmacology Transcriptional Activation - drug effects Up-Regulation - drug effects Virulence Factors, Bordetella - pharmacology
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