【摘要】在现在的文章,我们报导DR4或DR5overexpression戏剧性地在293T,MDA-MB-231和HCT-116房间以一种NF-魏B依赖者方式激活煽动性的cytokinesIL-8,TNF-伪,CCL20,MIP-2和MIP-1尾的版本。我们显示出调停受体的信号是的那死亡细胞外域无关,而DR4细胞内部的领域的overexpression的效果是少得多有势力。表明串联的TRADD-TRAF2-NIK-IKK伪/尾,在导致TNF的NF-魏B激活起一个必要作用,被发现涉及肿瘤坏死因素相关导致apoptosisligand(小道)调停受体的信号transduction。表明小径的FAD
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