Synergistic activation of intercellular adhesion molecule 1 (ICAM‐1) by TNF‐α and IFN‐γ is mediated by p65/p50 and p65/c‐Rel and interferon‐responsive factor Statlα (p91) that can be activated by both IFN‐γ and IFN‐α

FEBS Letters

P. Johnson, Judith¹  Jahnke, Andreas¹ 

[1] Institute of Immunology, Goethestr. 31, 80336 Munich, Germany

关键词: Genetics;    Cell adhesion molecule;    Promoter region;    Trans-activation;    Regulatory-sequence;    DNA-binding protein;    Cytokine;    EMSA;    electromobility shift assay;    GAF;    γ-activated factor;    GAS;    γ-activated sequence;    ICAM-1;    intercellular adhesion molecule-1;    IFN;    interferon;    IRE;    interferon-responsive element;    ISGF;    interferon α-stimulated gene factor;    RRBE;    Rel-related protein binding element;    TNF;    tumor necrosis factor;    TNF-R;    TNF-α receptor;   

DOI  :  10.1016/0014-5793(94)01130-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Human ICAM-1 expression is up-regulated by IFN-γ and TNF-α, 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-α-dependent complexes that bound to the NF-κB like sequence at −187 as p65/p50 and p65/c-Rel. The interferon responsive region at −75 was bound by a Statlα (p91) containing complex that was activated by both IFN-γ and IFN-α. Although both regions were required for synergism, no additional or enhanced binding complexes were observed.

【 授权许可】

Unknown