Cited by 317

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Autoinduction of transforming growth factor beta 1 is mediated by the AP-1 complex.

Kim, S J, Angel, P, Lafyatis, R, Hattori, K, Kim, K Y, Sporn, M B, Karin, M, Roberts, A B·1990·Molecular and Cellular Biology

Abstract

The multifunctional actions of transforming growth factor beta 1 (TGF-beta 1) indicate that it has a pivotal control function in many physiological and pathological processes. An important property of TGF-beta 1 is its ability to activate its own mRNA expression and thereby increase its own secretion. Two distinct regions of the promoter of the TGF-beta 1 gene are responsive to autoregulation: one 5' to the upstream transcriptional start site and another located between the two major start sites. In both promoter regions, autoinduction is mediated by binding of the AP-1 (Jun-Fos) complex. An important contribution to this positive regulation is the autoactivation of c-jun transcription by AP-1. Cotransfection of antisense c-jun or antisense c-fos expression vectors prevents TGF-beta 1 autoinduction. These results demonstrate that both components of the AP-1 complex are required for TGF-beta 1 autoinduction. Induction of jun expression by TGF-beta 1, as well as jun autoinduction, may amplify the action of TGF-beta 1 during normal development and oncogenesis.

Overview

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Crossref · 10.1128/mcb.10.4.1492

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1 of 1 references verified0 citation errors · 0 not checkable

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Metadata

Authors
Kim, S. J., Angel, P., Lafyatis, R., Hattori, K., Kim, K. Y., Sporn, M. B., Karin, M., & Roberts, A. B.
Venue
Molecular and Cellular Biology
Published
1990-04
Volume
10
Issue
4
Pages
1492-1497
ISSN
  • 0270-7306
  • 1098-5549
Cited by
317
References
1
Language
en

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