Transcription initiation sites and promoter structure of the human TRAIL-R3 gene

被引：7

作者：

de Almodóvar, CR

López-Rivas, A

Redondo, JM

Rodríguez, A

机构：

[1] Univ Autonoma Madrid, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain

[2] CSIC, Inst Parasitol & Biomed, E-18001 Granada, Spain

[3] Ctr Nacl Invest Cardiovasc, Madrid, Spain

来源：

FEBS LETTERS | 2002年 / 531卷 / 02期

关键词：

TRAIL-R3; decoy receptor; promoter structure; transcription; apoptosis; doxorubicin;

D O I：

10.1016/S0014-5793(02)03544-5

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

TRAIL-R3 is a decoy receptor for TRAIL (tumor necrosis factor-related apoptosis-inducing ligand), a member of the tumor necrosis factor ligand family. In several cell types decoy receptors inhibit TRAIL-induced apoptosis by binding TRAIL and preventing its binding to TRAIL pro-apoptotic receptors. Here we report the cloning of the promoter region of human TRAIL-R3 and the mapping of the transcriptional start sites. This gene contains a consensus TATA box and the minimal promoter lies within the first 33 nucleotides upstream of the transcription start site. Transient transfection assays of luciferase reporter plasmids demonstrate that human TRAIL-R3 promoter can be induced in doxorubicin-treated MCF-7 cells in a p53-independent manner. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：304 / 308

页数：5

共 35 条

[1] Oxidative damage of cardiomyocytes is limited by extracellular regulated kinases 1/2-mediated induction of cyclooxygenase-2 [J].