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FEBS Lett. 2006 Jan 23;580(2):669-76. Epub 2006 Jan 6.

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

Author information

1
Department of Pharmacology, Research Institute of Medical Sciences, Medical Research Center for Gene Regulation, Chonnam National University Medical School, Dong-Ku, Kwangju 501-190, Republic of Korea.

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 (GABPgamma) associates with the cytoplasmic domain of BAI2, and GABPalpha/gamma or GABPalpha/beta 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 GABPalpha and GABPgamma elicited increased VEGF expression before the onset of HIF-1alpha. Our results point out that BAI2 controls VEGF transcription through GABP under normal conditions and cerebral ischemia.

PMID:
16412436
DOI:
10.1016/j.febslet.2005.12.086
[Indexed for MEDLINE]
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