Wolfgang C D, Liang G, Okamoto Y, Allen A E, Hai T
Department of Medical Biochemistry, Ohio State Neurobiotechnology Center and the Ohio State Biochemistry Program, Ohio State University, Columbus, Ohio 43210, USA.
J Biol Chem. 2000 Jun 2;275(22):16865-70. doi: 10.1074/jbc.M909637199.
Previously, we demonstrated that ATF3 (activating transcription factor-3) is a stress-inducible gene, and the protein it encodes is a transcriptional repressor. In this report, we present evidence suggesting that ATF3 represses the transcription of its own gene. Interestingly, efficient repression requires a consensus ATF/cAMP-responsive element site in the promoter and a previously unidentified ATF3-binding site immediately downstream from the TATA box. Although this new site resembles the known ATF/cAMP-responsive element sequences at the flanking sequence, it differs from them at the center key residues. These observations indicate that ATF3 can tolerate variations in the center of the binding sites if the flanking sequences are favorable. The repression of the ATF3 promoter by its own gene product provides a mechanistic explanation, at least in part, for the transient expression pattern of the ATF3 gene upon stress induction.
此前，我们证明了激活转录因子3（ATF3）是一种应激诱导基因，其编码的蛋白质是一种转录抑制因子。在本报告中，我们提供的证据表明，ATF3可抑制其自身基因的转录。有趣的是，有效的抑制需要启动子中的一个共有ATF/cAMP反应元件位点以及TATA框下游紧邻的一个此前未鉴定的ATF3结合位点。尽管这个新位点在侧翼序列上类似于已知的ATF/cAMP反应元件序列，但在中心关键残基处与它们不同。这些观察结果表明，如果侧翼序列合适，ATF3能够容忍结合位点中心的变异。ATF3基因产物对ATF3启动子的抑制至少部分地为应激诱导后ATF3基因的瞬时表达模式提供了一种机制解释。
