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KDR — SP1

Text-mined interactions from Literome

Ishibashi et al., Nihon Ganka Gakkai Zasshi 1999 (Diabetic Retinopathy...) : AGEs and basic fibroblast growth factor (bFGF) induced expression of KDR in REC, and a transcription factor Sp 1 was involved in this process
Meissner et al., Circ Res 2004 : Constitutive Sp1 containing complex formation to this sequence is decreased by PPARalpha treatment, indicating that VEGFR2 gene expression is inhibited by repressing Sp1 site dependent DNA binding and transactivation
Komi et al., Cancer Sci 2009 (Carcinoma, Lewis Lung...) : beta-HIVS suppressed the phosphorylation but not the expression of extracellular signal regulated kinase, and an Sp1 dependent transactivation of the VEGFR2 and Tie2 promoters, thereby suppressing the proliferation of vascular endothelial and progenitor cells
Hata et al., J Biol Chem 1998 : Overexpression of Sp1 protein increased KDR promoter activity 3-fold in both EC and non-EC, whereas simultaneous co-expression of Sp3 attenuated this response
Giraudo et al., J Biol Chem 1998 : Mithramycin, an inhibitor of binding of nuclear transcription factor Sp1 to the promoter consensus sequence, blocked activation of VEGFR-2 , suggesting that the up-regulation of the receptor required Sp1 binding sites