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Journal of Biochemistry Advance Access originally published online on November 23, 2008
Journal of Biochemistry 2009 145(2):129-135; 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 Tanaka, Fumiko Itoh, Susumu Itoh* and Mitsuyasu Kato

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

*To whom correspondence should be addressed. Tel/Fax: +81-29-853-3944, E-mail: 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

Abbreviations: GATA-1, GATA binding protein 1; HEB, human B-HLH factor; Herp2, HES-related repressor protein 2; Id1, inhibitor of DNA binding 1; LMO2, LIM domain only 2; VEGFR2, vascular endothelial growth factor receptor 2


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