Abstract
To delineate the cis-acting elements of the proximal promoter responsible for cAMP-induced human renin gene transcription, 5'-flanking regions of the human renin gene were fused to a luciferase reporter gene and transfected in chorionic cells. Forskolin treatment induced the expression of luciferase by 2.4 fold when the reporter plasmid contained the promoter region (-582 to +16). Mutation or deletion of the CRE diminished (1.7 fold) but did not abolish cAMP-induced transcription, demonstrating that region containing the CRE and region containing a Pit-1 site were both necessary for cAMP maximal induction. Taken together, these results show that the cAMP response of the human renin gene may involve CREB binding the CRE and tissue-specific factors (from chorionic and kidney cell origin), different from Pit-1, that interact with the Pit-1 response DNA elements.
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