叔丁基对苯二酚在HepG2细胞中对γ-谷氨酰半胱氨酸合成酶轻亚基的诱导性表达不依赖于抗氧化反应元件。
Inducible expression of the gamma-glutamylcysteine synthetase light subunit by t-butylhydroquinone in HepG2 cells is not dependent on an antioxidant-responsive element.
作者信息
Galloway D C, McLellan L I
机构信息
Biomedical Research Centre, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, U.K.
出版信息
Biochem J. 1998 Dec 15;336 ( Pt 3)(Pt 3):535-9. doi: 10.1042/bj3360535.
Abstract
Mutation analysis of putative regulatory elements located in the 5'-flanking region of the gene encoding the regulatory subunit of gamma-glutamylcysteine synthetase (GLCLR) revealed that neither an antioxidant-responsive element (ARE) nor an activator protein-1 (AP-1) site regulates inducible expression by t-butylhydroquinone (tBHQ). The AP-1 site was found to modulate basal expression of GLCLR. A 42 bp region between nucleotides -303 and -344, not containing an ARE, was found to regulate inducible expression of GLCLR by tBHQ.
摘要
对位于γ-谷氨酰半胱氨酸合成酶调节亚基（GLCLR）编码基因5'侧翼区域的假定调控元件进行突变分析，结果显示抗氧化反应元件（ARE）和激活蛋白-1（AP-1）位点均不调节叔丁基对苯二酚（tBHQ）诱导的表达。发现AP-1位点可调节GLCLR的基础表达。在核苷酸-303至-344之间的一个42 bp区域（不包含ARE）被发现可调节tBHQ诱导的GLCLR表达。
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