Differential regulation of extracellular signal-related kinase phosphorylation by vitamin D3 analogs.

We examined the effects of vitamin D(3) on extracellular signal-related kinase (ERK). 1,25-(OH)(2)D(3), a form active in inducing transcription, caused rapid and transient ERK activation. 24R,25-(OH)(2)D(3), an inactive form, also activated ERK. In contrast, (22R)-22-methyl-20-epi-1,25-(OH)(2)D(3), a synthetic agonist of 1,25-(OH)(2)D(3), was not effective. These data provide evidence of selective roles of vitamin D(3) in nongenomic and genomic actions.