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Brain‐specific angiogenesis inhibitor 2 regulates VEGF through GABP that acts as a transcriptional repressor
Author(s) -
Jeong Byung Chul,
Kim Mi-Young,
Lee Ji Hee,
Kee Hae Jin,
Kho Dhong Hyo,
Han Kae Eun,
Qian Yong Ri,
Kim Jong-Keun,
Kim Kyung Keun
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.12.086
Subject(s) - repressor , angiogenesis , transcription (linguistics) , microbiology and biotechnology , transfection , promoter , transcriptional regulation , chemistry , cancer research , transcription factor , biology , gene expression , gene , biochemistry , linguistics , philosophy
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.