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.
Inoue
Erina
E
Nutritional Epidemiology Program, Bio-Index Project, National Institute of Health and Nutrition, Shinjuku, Tokyo, Japan.
Ishimi
Yoshiko
Y
Yamauchi
Jun
J
D000818:Animals; D016466:CHO Cells; D002117:Calcitriol / Q000494:pharmacology*; D002762:Cholecalciferol / Q000031:analogs & derivatives* / Q000494:pharmacology*; D006224:Cricetinae; D003412:Cricetulus; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D007700:Kinetics; D010766:Phosphorylation
D002762:Cholecalciferol; D048049:Extracellular Signal-Regulated MAP Kinases; D002117:Calcitriol