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ESE-1 is a novel transcriptional mediator of inflammation that interacts with NF-kappa B to regulate the inducible nitric-oxide synthase gene 总被引:1,自引:0,他引:1
Rudders S Gaspar J Madore R Voland C Grall F Patel A Pellacani A Perrella MA Libermann TA Oettgen P 《The Journal of biological chemistry》2001,276(5):3302-3309
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Activation of the selenoprotein SEPS1 gene expression by pro-inflammatory cytokines in HepG2 cells 总被引:1,自引:0,他引:1
Gao Y Hannan NR Wanyonyi S Konstantopolous N Pagnon J Feng HC Jowett JB Kim KH Walder K Collier GR 《Cytokine》2006,33(5):246-251
SEPS1 (also called selenoprotein S, SelS) plays an important role in the production of inflammatory cytokines and its expression is activated by endoplasmic reticulum (ER) stress. In this report, we have identified two binding sites for the nuclear factor kappa B in the human SEPS1 promoter. SEPS1 gene expression, protein levels and promoter activity were all increased 2-3-fold by TNF-alpha and IL-1beta in HepG2 cells. We have also confirmed that the previously proposed ER stress response element GGATTTCTCCCCCGCCACG in the SEPS1 proximate promoter is fully functional and responsive to ER stress. However, concurrent treatment of HepG2 cells with IL-1beta and ER stress produced no additive effect on SEPS1 gene expression. We conclude that SEPS1 is a new target gene of NF-kappaB. Together with our previous findings that SEPS1 may regulate cytokine production in macrophage cells, we propose a regulatory loop between cytokines and SEPS1 that plays a key role in control of the inflammatory response. 相似文献
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Steer JH Kroeger KM Abraham LJ Joyce DA 《The Journal of biological chemistry》2000,275(24):18432-18440
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P Oettgen K Kas A Dube X Gu F Grall U Thamrongsak Y Akbarali E Finger J Boltax G Endress K Munger C Kunsch T A Libermann 《The Journal of biological chemistry》1999,274(41):29439-29452
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Molecular mechanism of tumor necrosis factor-alpha production in 1-->3-beta-glucan (zymosan)-activated macrophages 总被引:3,自引:0,他引:3
Young SH Ye J Frazer DG Shi X Castranova V 《The Journal of biological chemistry》2001,276(23):20781-20787
The molecular details of 1-->3-beta-glucans, a fungal cell wall component, induced inflammatory responses are not well understood. In the present study, we conducted a systematic analysis of the molecular events leading to tumor necrosis factor (TNF)-alpha production after glucan stimulation of macrophages. We demonstrated that activation of nuclear factor kappaB (NF-kappaB) is essential in zymosan A (a source of 1-->3-beta-glucans)-induced TNF-alpha production in macrophages (RAW264.7 cells). Zymosan A-induced TNF-alpha protein production was associated with an increase in the TNF-alpha gene promoter activity. Activation of the TNF-alpha gene promoter was dependent on activation of NF-kappaB. Time course studies indicated that DNA binding activity of NF-kappaB preceded TNF-alpha promoter activity. Inhibition of NF-kappaB activation led to a dramatic reduction in both TNF-alpha promoter activity and TNF-alpha protein production in the response to zymosan A. Mutation of a major NF-kappaB binding site (kappa3) in the gene promoter resulted in a significant decrease in the induction of the gene promoter by zymosan A, while mutation of Egr or CRE sites failed to inhibit the response to zymosan. Together, these results strongly suggest that NF-kappaB is involved in signal transduction of 1-->3-beta-glucans-induced TNF-alpha expression. 相似文献
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A lipopolysaccharide-specific enhancer complex involving Ets, Elk-1, Sp1, and CREB binding protein and p300 is recruited to the tumor necrosis factor alpha promoter in vivo 总被引:11,自引:0,他引:11
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Tsai EY Falvo JV Tsytsykova AV Barczak AK Reimold AM Glimcher LH Fenton MJ Gordon DC Dunn IF Goldfeld AE 《Molecular and cellular biology》2000,20(16):6084-6094