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Journal of Biochemistry Advance Access published online on November 23, 2008
Journal of Biochemistry, doi:10.1093/jb/mvn158
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© The authors 2008. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.

Rapid Communication

TAL1/SCL relieves the E2-2-mediated repression of VEGFR2 promoter activity

Aya Tanaka1, Fumiko Itoh1, Susumu Itoh1,2 and Mitsuyasu Kato1

1Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan

2Corresponding author: Dr. Susumu Itoh. Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan, Tel/Fax: +81-29-853-3944; Email: sitoh{at}md.tsukuba.ac.jp

Received November 9, 2008; Accepted November 11, 2008


  Abstract

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.

Key Words: angiogenesis, E2-2, endothelial cell, SCL/TAL1, VEGFR2


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