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Research Article Free access | 10.1172/JCI117482

C/EBP beta regulation of the tumor necrosis factor alpha gene.

R M Pope, A Leutz, and S A Ness

Department of Medicine, Northwestern University, Chicago, Illinois.

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Department of Medicine, Northwestern University, Chicago, Illinois.

Find articles by Leutz, A. in: PubMed | Google Scholar

Department of Medicine, Northwestern University, Chicago, Illinois.

Find articles by Ness, S. in: PubMed | Google Scholar

Published October 1, 1994 - More info

Published in Volume 94, Issue 4 on October 1, 1994
J Clin Invest. 1994;94(4):1449–1455. https://doi.org/10.1172/JCI117482.
© 1994 The American Society for Clinical Investigation
Published October 1, 1994 - Version history
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Abstract

Activated macrophages contribute to chronic inflammation by the secretion of cytokines and proteinases. Tumor necrosis factor alpha (TNF alpha) is particularly important in this process because of its ability to regulate other inflammatory mediators in an autocrine and paracrine fashion. The mechanism(s) responsible for the cell type-specific regulation of TNF alpha is not known. We present data to show that the expression of TNF alpha is regulated by the transcription factor C/EBP beta (NF-IL6). C/EBP beta activated the TNF alpha gene promoter in cotransfection assays and bound to it at a site which failed to bind the closely related protein C/EBP alpha. Finally, a dominant-negative version of C/EBP beta blocked TNF alpha promoter activation in myeloid cells. Our results implicate C/EBP beta as an important regulator of TNF alpha by myelomonocytic cells.

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