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A Short Region Containing an AP‐1 Binding Site Is Essential for Transforming Growth Factor‐beta‐Induced c‐jun Gene Expression in Osteoblastic Cells
Author(s) -
Hata Satoshi,
Shimizu Toshikatsu,
Fujimoto Masafumi
Publication year - 2000
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/713803612
Subject(s) - ap 1 transcription factor , microbiology and biotechnology , transcription factor , transfection , c jun , biology , signal transduction , transforming growth factor beta , r smad , reporter gene , transforming growth factor , gene expression , gene , tgf beta receptor 2 , regulation of gene expression , chemistry , endoglin , biochemistry , stem cell , cd34
Transforming growth factor‐beta (TGF‐beta) is a multifunctional regulatory peptide that elicits different responses in different cell types. Much remains unknown about the pathway of intracellular TGF‐beta signal transduction, but TGF‐beta is known to induce expression of several genes by way of the transcription factor AP‐1. We studied the mechanism that mediates TGF‐beta?induced gene expression of c‐jun, a component of AP‐1, in MC3T3‐E1 osteoblastic cells. To map in detail the corresponding responsive elements in the rat c‐jun promoter, we generated a series of 5′ deletion promoter/luciferase reporter gene constructs. Transient cell transfection assays identified the region located between positions ‐79 and ‐59 as being critical for the TGF‐beta response and for the basal activity of the promoter. Gel mobility shift assays indicated specific binding of nuclear proteins to this 21‐bp region of the c‐jun promoter containing an AP‐1 binding site. These results show that the AP1?dependent mechanism is involved in TGF‐beta?induced increase of c‐jun induction, suggesting positive autoregulation of AP‐1.