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つくばリポジトリ (Tulips-R) >
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Biochemical and biophysical research communications >
Please use this identifier to cite or link to this item:
http://hdl.handle.net/2241/98153
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| Title: | Suppression of MafA-dependent transcription by transforming growth factor-b signaling |
| Authors: | Matsumura, Haruka
Kudo, Takashi
Harada, Ayako
Esaki, Ritsuko
Suzuki, Hiroyuki
Kato, Mitsuyasu
Takahashi, Satoru
工藤, 崇
高橋, 智 |
| Issue Date: | Dec-2007 |
| Publisher: | Elsevier Inc. |
| Journal Title: | Biochemical and biophysical research communications |
| Volume: | 364 |
| Issue: | 1 |
| Start Page: | 151 |
| End Page: | 156 |
| DOI: | 10.1016/j.bbrc.2007.09.110 |
| PMID: | 17927952 |
| Abstract: | MafA is a basic leucine zipper (b-Zip) type transcription factor that binds to the insulin promoter and regulates insulin transcription
synergistically with Pdx-1 and NeuroD. Transforming growth factor-b (TGF-b) signaling has been reported to regulate activity of b-Zip
transcription factor such as ATF-2 and acts as an important regulator of insulin gene transcription and pancreatic b cell maintenance. To
investigate the relationship between MafA-dependent transcriptional activation and TGF-b signaling, we examined the effects of TGF-b
signal on MafA-dependent transactivation of the rat insulin II gene promoter (RIPII-251) and a synthetic MafA-dependent promoter.
MafA-dependent activation of the reporters was inhibited in the presence of Smad2/Smad4 or Smad3/Smad4 and a constitutively active
TGF-b type I receptor and this inhibition was dependent upon the presence of MafA. Co-immunoprecipitation analyses revealed that
MafA physically interacts with Smad2 or Smad3. These results suggest that MafA-dependent transcriptional activation is negatively regulated
by TGF-b signaling. |
| URI: | http://hdl.handle.net/2241/98153 |
| Rights: | ©2007 Elsevier Inc. |
| Text Version: | author |
| Appears in Collections: | Biochemical and biophysical research communications
工藤 崇 (Kudo Takashi)
高橋 智 (Takahashi Satoru)
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