SYNERGISTIC ACTIVATION OF INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) BY TNF-ALPHA AND IFN-GAMMA IS MEDIATED BY P65/P50 AND P65/1C-REL AND INTERFERON-RESPONSIVE FACTOR STAT1-ALPHA (P91) THAT CAN BE ACTIVATED BY BOTH IFN-GAMMA AND IFN-ALPHA
SYNERGISTIC ACTIVATION OF INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) BY TNF-ALPHA AND IFN-GAMMA IS MEDIATED BY P65/P50 AND P65/1C-REL AND INTERFERON-RESPONSIVE FACTOR STAT1-ALPHA (P91) THAT CAN BE ACTIVATED BY BOTH IFN-GAMMA AND IFN-ALPHA
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DOI：
10.1016/0014-5793(94)01130-3
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发表时间：
1994-11-07
期刊：
影响因子：
3.5
通讯作者：
JOHNSON, JP
中科院分区：
文献类型：
--
作者：
JAHNKE, A;JOHNSON, JP
人ICAM-1的表达被IFN-γ和TNF-α上调，并通过两者的组合协同增加。ICAM-1/荧光素酶构建体的瞬时表达导致介导细胞因子应答的调节区的定义，并表明两者对于协同作用是必需的。免疫化学电迁移率变动分析鉴定了在-187处与NF-κ B样序列结合的TNF-α依赖性复合物为p65/p50和p65/c-Rel。在-75处的干扰素应答区被含有Statl α（p91）的复合物结合，所述复合物被IFN-γ和IFN-α两者激活。虽然这两个区域都需要协同作用，但没有观察到额外的或增强的结合复合物。
Human ICAM-1 expression is up-regulated by IFN-gamma and TNF-alpha, and synergistically increased by a combination of both. Transient expression of ICAM-1/luciferase constructs led to definition of the regulatory regions mediating the cytokine response and showed that both are necessary for synergism. Immunochemical electromobility shift assays identified the TNF-alpha-dependent complexes that bound to the NF-kappa B like sequence at -187 as p65/p50 and p65/c-Rel. The interferon responsive region at -75 was bound by a Statl alpha (p91) containing complex that was activated by both IFN-gamma and IFN-alpha. Although both regions were required for synergism, no additional or enhanced binding complexes were observed.