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|Title:||Molecular structure and transcriptional regulation by nuclear factor-kappa B of the mouse kinin B-1 receptor gene|
|Authors:||Merino, V. F.|
Silva, J. A.
Araujo, R. C.
Bascands, J. L.
Schanstra, J. P.
Pesquero, J. B.
Universidade Federal de São Paulo (UNIFESP)
Univ Mogi Cruzes
Max Delbruck Ctr Mol Med
mouse kinin B
multiple transcription start sites
nuclear factor-kappa B (NF-kappa B)
|Publisher:||Walter de Gruyter & Co|
|Citation:||Biological Chemistry. Berlin: Walter de Gruyter & Co, v. 386, n. 6, p. 515-522, 2005.|
|Abstract:||Kinins are important mediators in cardiovascular homeostasis, inflammation, and nociception. Two kinin receptors have been described, B-1 and B-2. the B-1 receptor is normally absent in healthy tissues, but is highly induced under pathological conditions. To understand the molecular mechanism of B-1 receptor up-regulation, we determined the mouse B-1 receptor gene structure, isolated and characterized the promoter region and studied its transcriptional regulation. the mouse B-1 receptor gene contains two exons (with the entire coding region located in the second exon) and a TATA-less promoter with multiple transcription start sites. A 7.7-kbp portion of the 5'-flanking region was examined for promoter activity in vascular smooth muscle cells (VSMCs). A minimal 92-bp fragment, located immediately upstream of the transcription start region, exerted basal and lipopolysaccharide (LPS)-inducible transcription activity in the sense and antisense orientation, and was thereby identified as an enhancer element. Nuclear extracts from VSMCs showed basal and LPS-inducible binding activity of nuclear factor (NF)-kappa B at this sequence. B-1 receptor transcription activation in response to LPS was abolished by cotransfection with I kappa B alpha Delta N, an NF-kappa B repressor. in summary, our results reveal the structure of the mouse B-1 receptor gene and the involvement of NF-kappa B in the inducible mouse kinin B-1 receptor expression under pathological conditions.|
|Appears in Collections:||Em verificação - Geral|
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