Jahnke A, Johnson J P
Institute of Immunology, Munich, Germany.
FEBS Lett. 1994 Nov 7;354(2):220-6. doi: 10.1016/0014-5793(94)01130-3.
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 Stat1 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.
人细胞间黏附分子-1（ICAM-1）的表达受γ干扰素（IFN-γ）和肿瘤坏死因子-α（TNF-α）上调，二者联合作用时协同性增强。ICAM-1/荧光素酶构建体的瞬时表达确定了介导细胞因子应答的调控区域，并表明二者对协同作用均是必需的。免疫化学电泳迁移率变动分析确定，与-187处NF-κB样序列结合的TNF-α依赖性复合物为p65/p50和p65/c-Rel。-75处的干扰素反应区域由一种含Stat1α（p91）的复合物结合，该复合物被IFN-γ和IFN-α激活。虽然协同作用需要这两个区域，但未观察到额外或增强的结合复合物。
