Inducible expression of the gamma-glutamylcysteine synthetase light subunit by t-butylhydroquinone in HepG2 cells is not dependent on an antioxidant-responsive element.
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.
Galloway
D C
DC
Biomedical Research Centre, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, U.K.
McLellan
L I
LI
D000975:Antioxidants / Q000494:pharmacology*; D001483:Base Sequence; D004247:DNA / Q000378:metabolism; D004742:Enhancer Elements, Genetic; D004790:Enzyme Induction; D005721:Glutamate-Cysteine Ligase / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D006873:Hydroquinones / Q000494:pharmacology*; D008969:Molecular Sequence Data; D011487:Protein Conformation; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014407:Tumor Cells, Cultured
D000975:Antioxidants; D006873:Hydroquinones; D018808:Transcription Factor AP-1; D004247:DNA; C018855:2-tert-butylhydroquinone; D005721:Glutamate-Cysteine Ligase