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lüll Regulation of intercellular adhesion molecule-1 (CD54) gene expression Roebuck KA; Finnegan AJ Leukoc Biol 1999[Dec]; 66 (6): 876-88Intercellular adhesion molecule-1 (ICAM-1, CD54) is an inducible cell adhesion glycoprotein of the immunoglobulin supergene family expressed on the surface of a wide variety of cell types. ICAM-1 interactions with the beta2 integrins CD11a/CD18 (LFA-1) and CD11b/CD18 (MAC-1) on the surface of leukocytes are important for their transendothelial migration to sites of inflammation and their function as costimulatory molecules for T cell activation. ICAM-1 is constitutively expressed on the cell surface and is up-regulated in response to a variety of inflammatory mediators, including proinflammatory cytokines, hormones, cellular stresses, and virus infection. These stimuli increase ICAM-1 expression primarily through activation of ICAM-1 gene transcription. During the past decade much has been learned about the cell type- and stimulus-specific transcription of ICAM-1. The architecture of the ICAM-1 promoter is complex, containing a large number of binding sites for inducible transcription factors, the most important of which is nuclear factor-kappa B (NF-kappaB). NF-kappaB acts in concert with other transcription factors and co-activators via specific protein-protein interactions, which facilitate the assembly of distinct stereospecific transcription complexes on the ICAM-1 promoter. These transcription complexes presumably mediate the induction of ICAM-1 expression in different cell types and in response to different stimuli. In this review, we summarize our current understanding of ICAM-1 gene regulation with a particular emphasis on the transcription factors and signal transduction pathways critical for the cell type- and stimulus-specific activation of ICAM-1 gene transcription.|Animals[MESH]|Base Sequence[MESH]|Gene Expression Regulation/*immunology[MESH]|Humans[MESH]|Intercellular Adhesion Molecule-1/*biosynthesis/*genetics[MESH]|Molecular Sequence Data[MESH]|Signal Transduction/immunology[MESH] |