Abstract

A growing body of evidence demonstrates that elevated expression of the endothelial cell adhesion molecules E-selectin, VCAM-1 and ICAM-1 at sites of inflammation in vivo is due in whole or part to the upregulation of transcription of their respective genes. Pharmacologic antagonism of transcription from these genes may therefore represent a novel approach to the development of anti-inflammatory therapeutics. This paper reviews our current understanding of nuclear factors which act to regulate the transcriptional activity of the E-selectin, VCAM-1 and ICAM-1 genes, and discusses that evidence which suggests that the nuclear transcription factor NF-kappa B acts as a dominant regulator of transcription from these genes.

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