共查询到20条相似文献,搜索用时 15 毫秒
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The functional importance of a cap site-proximal region of the human prointerleukin 1 beta gene is defined by viral protein trans-activation.
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G W Hunninghake B G Monks L J Geist M M Monick M A Monroy M F Stinski A C Webb J M Dayer P E Auron M J Fenton 《Molecular and cellular biology》1992,12(8):3439-3448
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H Zorbas T Rein A Krause K Hoffmann E L Winnacker 《The Journal of biological chemistry》1992,267(12):8478-8484
Methylation interference and missing contact analyses demonstrate that nuclear factor I (NF I) recognizes an NF I-like site (5'-GGG(N)6GCCAG-3') within the alpha-globin promoter rather than the adjacent CCAAT box. Consistent with this, mutations within the CCAAT box do not alter significantly the affinity and specificity of the interaction whereas elimination of the 5'-GGG-3' half-site of the recognition sequence reduces the DNA binding strength of NF I by 2 orders of magnitude down to the range of unspecific interaction. On the other hand, the mutated alpha-globin promoter sequence that is no longer bound by NF I, although it retains an intact CCAAT box, interacts specifically with a protein component from nuclear extracts of HeLa cells. From these results we conclude that NF I is not the factor that interacts with the CCAAT box and that the second half of the canonical 5'-TGG(N)6GCCAA-3' NF I binding site cannot be regarded as identical with the CCAAT promoter element, as suggested previously. 相似文献
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Perrella MA Pellacani A Wiesel P Chin MT Foster LC Ibanez M Hsieh CM Reeves R Yet SF Lee ME 《The Journal of biological chemistry》1999,274(13):9045-9052
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Dynamic binding of Ku80, Ku70 and NF90 to the IL-2 promoter in vivo in activated T-cells 总被引:2,自引:0,他引:2
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Shi L Qiu D Zhao G Corthesy B Lees-Miller S Reeves WH Kao PN 《Nucleic acids research》2007,35(7):2302-2310
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Among a panel of 21 cytokines (IL-1alpha, -1beta, -2-13, and -15-18; interferon-gamma; granulocyte-macrophage colony-stimulating factor; and tumor necrosis factor alpha), we have recently observed that IL-17A is the most potent inducer for human beta-defensin 2 (hBD-2) in conducting airway epithelial cells (Kao, C. Y., Chen, Y., Thai, P., Wachi, S., Huang, F., Kim, C., Harper, R. W., and Wu, R. (2004) J. Immunol. 173, 3482-3491). The molecular basis of this regulation is not known. In this study, we demonstrated a coordinated degradation of inhibitory kappaB(IkappaB)-alpha followed by a nuclear translocation of p50 and p65 NF-kappaB subunits and their binding to NF-kappaB sites of hBD-2 promoter region. With site-directed mutagenesis, we demonstrated the requirement of two proximal NF-kappaB binding sites (pkappaB1, -205 to -186; pkappaB2, -596 to -572) but not the distal site (dkappaB, -2193 to -2182) in supporting IL-17A-induced hBD-2 promoter activity. These results are consistent with the data of the chromatin immunoprecipitation assay, which showed enhanced p50 binding to these pkappaB sites but not the dkappaB site in cells after IL-17A treatment. We also found that the NF-kappaB binding cofactor, IkappaB-zeta, was up-regulated by IL-17A, and the knockdown of IkappaB-zeta significantly diminished the IL-17A-induced hBD-2 expression. This is the first demonstration of the involvement of two proximal NF-kappaB sites and IkappaB-zeta in the regulation of hBD-2 by IL-17A, two important genes responsible for host defense. 相似文献
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Yin-Yang 1 activates interleukin-4 gene expression in T cells. 总被引:2,自引:0,他引:2
J Guo V Casolaro E Seto W M Yang C Chang M C Seminario J Keen S N Georas 《The Journal of biological chemistry》2001,276(52):48871-48878
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M F Iademarco J J McQuillan G D Rosen D C Dean 《The Journal of biological chemistry》1992,267(23):16323-16329
Vascular cell adhesion molecule-1 (VCAM-1) was first identified as a protein that appears on the surface of endothelial cells after exposure to inflammatory cytokines. Through interaction with its integrin counter receptor VLA-4, VCAM-1 mediates cell-cell interactions important for immune function. We have cloned and begun characterization of the promoter for the VCAM-1 gene. In a series of transfection assays into human umbilical vein endothelial cells (HUVECs), we find that silencers between positions -1.641 kilobases and -288 base pairs restrict promoter activity, and that treatment with tumor necrosis factor-alpha overcomes this inhibition and activates the promoter through two NF kappa B sites located at positions -77 and -63 base pairs of the VCAM-1 gene. This responsiveness appears cell-specific since constructs containing the VCAM-1 NF kappa B sites are not responsive to tumor necrosis factor alpha in the T-cell line Jurkat. The two VCAM-1 NF kappa B sites, which differ slightly in their sequence, form distinct complexes in gel retardation assays, suggesting that they interact with different NF kappa B-site binding proteins. The distribution of these proteins could then control activity of the NF kappa B sites. We conclude that the pattern of VCAM-1 expression in HUVECs is controlled by a combination of these silencers and NF kappa B sites. 相似文献
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