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Kcnb1  expression is down-regulated in certain types of cardiomyopathy. As a first step towards understanding  Kcnb1  regulation, we determined its genomic structure and characterized its 5′-regulatory region. Two species of  Kcnb1  mRNA were found to arise from alternative usage of two highly GC-rich promoters (P1, P2). While transcripts arising from P1 were mainly detected in brain, P2 transcripts were highly expressed in heart and brain. Core regulatory regions were characterized for P1 and P2. The mutation of a potential Nur77/Nurr1/NOR-1 binding site, NBRE Kcnb1 , conserved in both human and mouse, resulted in a significant decrease in basal P2 promoter activity. Luciferase activities of the longest promoter-reporter construct reflected the level of endogenous  Kcnb1  mRNA in myoblast, smooth muscle, and pituitary cell lines. Hyperosmolarity increased  Kcnb1  mRNA concentration two-fold, mainly at the transcriptional level in clonal pituitary cells. These findings provide a basis for future studies of (post)transcriptional mechanism(s) down-regulating  Kcnb1  expression in a variety of cardiomyopathies and point towards a possible involvement of  Kcnb1  in pituitary cell excitability and secretory activity regulated by osmolarity.

The K + channel gene, Kcnb1 : genomic structure and characterization of its 5′-regulatory region as part of an overlapping gene group