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complex(p(HGNC:CTNNB1),g(HGNC:VEGFA))
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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To determine whether activation of the Wnt pathway directly up-regulates the VEGF promoter, an oncogenic ß-cateninS37A was transfected with the 2.8-kb VEGF-pGL2 reporter into HeLa cells. A critical serine phosphorylation site at amino acid 37 that ordinarily targets ß-catenin for degradation has been mutated (10) . Fig. 1D. Citation illustrates a linear dose response to the effects of ß-cateninS37A. The peak response was observed when 1.25 µg of expression vector was cotransfected with 0.75 µg of reporter vector, resulting in a >30-fold stimulation of VEGF promoter activity. In independent studies, HeLa cells were treated with 25 mM LiCl, an inhibitor of GSK-3ß kinase activity. GSK-3ß is a negative regulator of Wnt signaling, and inhibiting GSK-3ß with LiCl resulted in a 2.2-fold increase in VEGF promoter activity. Collectively, these findings indicate that activation of Wnt signaling up-regulates VEGF expression in colonic neoplasia. (from full text)
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