Differential Regulation of Extracellular Signal-Related Kinase Phosphorylation by Vitamin D₃ Analogs

Abstract

We examined the effects of vitamin D₃ on extracellular signal-related kinase (ERK). 1,25-(OH)₂D₃, a form active in inducing transcription, caused rapid and transient ERK activation. 24R,25-(OH)₂D₃, an inactive form, also activated ERK. In contrast, (22R)-22-methyl-20-epi-1,25-(OH)₂D₃, a synthetic agonist of 1,25-(OH)₂D₃, was not effective. These data provide evidence of selective roles of vitamin D₃ in nongenomic and genomic actions.