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A T-cell enhancer cooperates with NF-kappa B to yield cytokine induction of E-selectin gene transcription in endothelial cells
ELAM1 (endothelial leukocyte adhesion molecule 1, also known as E-selectin) is a highly tissue-specific adhesion molecule that is transiently and exclusively expressed on cytokine-induced endothelial cells. We have identified two proximal ELAM1 promoter elements and their DNA-binding factors that ar...
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Published in: | The Journal of biological chemistry 1992-11, Vol.267 (31), p.22385-22391 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | ELAM1 (endothelial leukocyte adhesion molecule 1, also known as E-selectin) is a highly tissue-specific adhesion molecule
that is transiently and exclusively expressed on cytokine-induced endothelial cells. We have identified two proximal ELAM1
promoter elements and their DNA-binding factors that are, in addition to NF-kappa B, essential for ELAM1 transcription. Mutation
of either element in promoter constructs carrying the first 383 nucleotides of the ELAM1 promoter markedly diminshed the expression
of a fused chloramphenicol acetyltransferase reporter gene. Although multimers of either element failed to display enhancer
activity on its own, fusion of the most upstream of these to the NF-kappa B element had a strong stimulatory effect. This
site, ACATCAT, is recognized by a factor we have called NF-ELAM1. The site corresponds to NF-ELAM1's preferential binding
sequence (A/T)CA(G/T)CA(G/T) as determined in a target definition assay. This element is identical to the T-cell delta A enhancer
found in the T-cell receptor-alpha, -beta, and CD3 delta genes. Our results suggest that the delta A/NF-ELAM1 element can
function as a modulator of NF-kappa B in endothelial cells both as well as a T-cell enhancer. |
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ISSN: | 0021-9258 1083-351X |
DOI: | 10.1016/S0021-9258(18)41683-3 |