-
The early-immediate gene EGR-1 is induced by transforming growth factor-betaand mediates stimulation of collagen gene expressionChen, Shu-Jen ...Transforming growth factor-beta (TGF-I3) stimulates collagen synthesis and accumulation, and aberrant TGF-13 signaling is implicated in pathological organ fibrosis. Regulation of Type I procollagen ... gene (COL1A2) transcription by TGF-beta involves the canonical Smad signaling pathway as well as additional protein and lipid kinases, coactivators and DNA-binding transcription factors that constitute alternate non-Smad pathways. Using Affymetrix microarrays to detect cellular genes whose expression is regulated by Smad3, we identified early growth response factor-1 (Egr-1) as a novel Smad3-inducible gene. Previous studies implicated Egr-1 in cell growth, differentiation and survival. We found that TGF-beta induced rapid and transient accumulation of Egr-1 protein and mRNA in human skin fibroblasts. Intransient transfection assays, TGF-beta stimulated the activity of the Egr-1gene promoter, as well as that of a minimal Egr-1responsive reporter construct. Furthermore, TGF-beta enhanced endogenous Egr-1 interaction with a consensus Egr-1 binding site element, and with GC-rich DNA sequences of the human COL1A2 promoter in vitro and in vivo. Forced expression of Egr-1 by itself caused doseIependent up-regulation of COL1A2 promoter activity, and further enhanced the stimulation nduced by TGF-beta. In contrast, the TGF-betaResponse was abrogated when the Egr-1 Binding sites of the COL1A2 promoter were nutated or deleted. Furthermore, Egr-1leficient embryonic mouse fibroblasts showed attenuated TGF-beta responses despite intact Smad activation, and forced expression of ectopic Egr-1 in these cells could restore COL1A2 stimulation in a dose-dependent manner. Taken together, these findings identify Egr-1 as a novel intracellular TGF-beta target that is necessary for maximal stimulation of collagen gene expression in fibroblasts. (Abstract truncated at 2000 characters)Source: The Journal of biological chemistry. - ISSN 0021-9258 (Letn. 281, št. 30, 2006, str. 21183-21197)Type of material - article, component partPublish date - 2006Language - englishCOBISS.SI-ID - 21381849
Author
Chen, Shu-Jen |
Ning, Hongyan |
Ishida, Wataru |
Sodin-Šemrl, Snežna, 1962- |
Takagawa, Shinsuke |
Mori, Yasuji |
Varga, John
Topics
Transforming Growth Factor Beta |
Biosynthesis |
Collagen |
Biosynthesis |
Metabolism |
Gene Expression Regulation |
Fibroblasts |
Metabolism |
Signal Transduction |
Base Sequence |
Molecular Sequence Data |
Oligonucleotide Probes |
Mice |
Fibroblasti |
Gensko izražanje, regulacija |
Kolagen |
Signal, prevajanje |
Transformacijski, rastni faktor beta |
Baze, zaporedje |
Miši |
Molekulsko zaporedje, podatki |
Oligonukleotidne sonde
![loading ... loading ...](themes/default/img/ajax-loading.gif)
![loading ... loading ...](themes/default/img/ajax-loading.gif)
![loading ... loading ...](themes/default/img/ajax-loading.gif)
![loading ... loading ...](themes/default/img/ajax-loading.gif)
Shelf entry
Permalink
- URL:
Impact factor
Access to the JCR database is permitted only to users from Slovenia. Your current IP address is not on the list of IP addresses with access permission, and authentication with the relevant AAI accout is required.
Year | Impact factor | Edition | Category | Classification | ||||
---|---|---|---|---|---|---|---|---|
JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
Select the library membership card:
DRS, in which the journal is indexed
Database name | Field | Year |
---|
Links to authors' personal bibliographies | Links to information on researchers in the SICRIS system |
---|---|
Chen, Shu-Jen | ![]() |
Ning, Hongyan | ![]() |
Ishida, Wataru | ![]() |
Sodin-Šemrl, Snežna, 1962- | 26481 |
Takagawa, Shinsuke | ![]() |
Mori, Yasuji | ![]() |
Varga, John | ![]() |
Select pickup location:
Material pickup by post
Notification
Subject headings in COBISS General List of Subject Headings
Select pickup location
Pickup location | Material status | Reservation |
---|
Please wait a moment.