TAL1/SCL relieves the E2-2-mediated repression of VEGFR2 promoter activity.
The basic helix-loop-helix (bHLH) protein TAL1/SCL is essential for embryonic-vascular development. TAL1/SCL regulates the activation of endothelial cells by binding directly or indirectly to DNA sequences in critical target genes. We recently demonstrated that E-box protein E2-2 blocks endothelial cell activation via perturbation of VEGFR2 promoter activity. Herein, we report that TAL1/SCL interacts with E2-2 and inhibits E2-2-mediated effects on reporter activity. Mutational analysis revealed that the HLH domain of TAL1/SCL, but not its basic region, is required for interaction with E2-2. Importantly, TAL1/SCL relieves the E2-2-mediated repression of VEGFR2 reporter activity in endothelial cells. Our data elaborate on the bHLH protein interactions that regulate endothelial cell activation.
Tanaka
Aya
A
Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.
Itoh
Fumiko
F
Itoh
Susumu
S
Kato
Mitsuyasu
M
D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000378:metabolism*; D019556:COS Cells; D002522:Chlorocebus aethiops; D042783:Endothelial Cells / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D011401:Promoter Regions, Genetic / Q000235:genetics*; D051820:TCF Transcription Factors / Q000378:metabolism*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000235:genetics* / Q000378:metabolism
D051792:Basic Helix-Loop-Helix Proteins; D051820:TCF Transcription Factors; D040301:Vascular Endothelial Growth Factor Receptor-2