Abstract
Biliverdin reductase (BVR) functions in cell signaling through three distinct tracks: a dual-specificity kinase that functions in the insulin receptor/MAPK pathways (25, 29, 51); a bzip-type transcription factor for ATF-2/CREB and HO-1 regulation (1, 25); and a reductase that catalyzes the conversion of biliverdin to bilirubin (27). These, together with the protein’s primary and secondary features, intimately link BVR to the entire spectrum of cell-signaling cascades.