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C Jobin C A Bradham M P Russo B Juma A S Narula D A Brenner R B Sartor 《Journal of immunology (Baltimore, Md. : 1950)》1999,163(6):3474-3483
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Tumor necrosis factor and interleukin-1 lead to phosphorylation and loss of I kappa B alpha: a mechanism for NF-kappa B activation. 总被引:41,自引:19,他引:22 下载免费PDF全文
Nuclear factor kappa B (NF-kappa B) is a critical regulator of several genes which are involved in immune and inflammation responses. NF-kappa B, consisting of a 50-kDa protein (p50) and a 65-kDa protein (p65), is bound to a cytoplasmic retention protein called I kappa B. Stimulation of cells with a variety of inducers, including cytokines such as tumor necrosis factor and interleukin-1, leads to the activation and the translocation of p50/65 NF-kappa B into the nucleus. However, the in vivo mechanism of the activation process remains unknown. Here, we provide the first evidence that the in vivo mechanism of NF-kappa B activation is through the phosphorylation and subsequent loss of its inhibitor, I kappa B alpha. We also show that both I kappa B alpha loss and NF-kappa B activation are inhibited in the presence of antioxidants, demonstrating that the loss of I kappa B alpha is a prerequisite for NF-kappa B activation. Finally, we demonstrate that I kappa B alpha is rapidly resynthesized after loss, indicating that an autoregulatory mechanism is involved in the regulation of NF-kappa B function. We propose a mechanism for the activation of NF-kappa B through the modification and loss of I kappa B alpha, thereby establishing its role as a mediator of NF-kappa B activation. 相似文献
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Fitzgerald KA Bowie AG Skeffington BS O'Neill LA 《Journal of immunology (Baltimore, Md. : 1950)》2000,164(4):2053-2063
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Tabary O Escotte S Couetil JP Hubert D Dusser D Puchelle E Jacquot J 《Journal of immunology (Baltimore, Md. : 1950)》2000,164(6):3377-3384
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