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Brain-specific angiogenesis inhibitor 2 regulates VEGF through GABP that acts as a transcriptional repressor

Authors
 Byung Chul Jeong  ;  Mi-Young Kim  ;  Ji Hee Lee  ;  Hae Jin Kee  ;  Dhong Hyo Kho  ;  Kae Eun Han  ;  Yong Ri Qian  ;  Jong-Keun Kim  ;  Kyung Keun Kim 
Citation
 FEBS LETTERS, Vol.580(2) : 669-676, 2006 
Journal Title
 FEBS LETTERS 
ISSN
 0014-5793 
Issue Date
2006
MeSH
Animals ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Cell Line ; GA-Binding Protein Transcription Factor/genetics ; GA-Binding Protein Transcription Factor/metabolism* ; Humans ; Membrane Proteins ; Mice ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism* ; Protein Subunits/genetics ; Protein Subunits/metabolism ; Rats ; Rats, Sprague-Dawley ; Repressor Proteins/genetics ; Repressor Proteins/metabolism* ; Transcription, Genetic* ; Two-Hybrid System Techniques ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism*
Keywords
Brain-specific angiogenesis inhibitor 2 ; Vascular endothelial growth factor ; GA-binding protein ; Cerebral ischemia ; Transcriptional repressor
Abstract
Previously, we reported that decreased brain-specific angiogenesis inhibitor 2 (BAI2) induced increased VEGF expression. The regulatory mechanisms for this process are not understood. Here we show that GA-binding protein gamma (GABPγ) associates with the cytoplasmic domain of BAI2, and GABPα/γ or GABPα/β works as a transcriptional repressor of VEGF in SHSY5Y cells. Transcriptional activity of wild-type VEGF promoter was significantly increased in anti-sense BAI2-transfected cells, but not that of VEGF promoter harboring mutated GABP sites. In in vivo focal cerebral ischemia model, the decrease in BAI2 accompanied by decreased GABPα and GABPγ elicited increased VEGF expression before the onset of HIF-1α. Our results point out that BAI2 controls VEGF transcription through GABP under normal conditions and cerebral ischemia.
Files in This Item:
T200605426.pdf Download
DOI
10.1016/j.febslet.2005.12.086
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Mi Young(김미영)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/111114
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