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“Pretreatment with retinoic acid resulting in partial neuronal differentiation greatly enhanced the cells' sensitivity towards adenylyl cyclase stimulation by prostaglandin E1 , and its inhibition by morphine and alpha 2-agonists.”
European journal of pharmacology • 1992 | View Paper
“Although the simultaneous addition of PGE1 or PGE2 (10(-8)-10(-6) M) produced no enhancement of RA-induced TGase activity, adding PGE1 or PGE2 24 or 48 h following RA treatments produced an enhancement of TGase activity.”
“Although all four differentiation factors caused morphological changes towards a neuronal phenotype, only retinoic acid dramatically enhanced cyclic AMP accumulation, specifically upon stimulation with prostaglandin E1 (PGE,).”
“ Retinoic acid inhibited … PGE1 in a dose-dependent manner in the range between 0.1 and 10 nM. Retinoic acid also suppressed the IL-6 synthesis stimulated … activator of protein kinase C. The IL-6 synthesis induced by cholera toxin, forskolin or dibutyryl cAMP was inhibited by retinoic acid.”
Prostaglandins, leukotrienes, and essential fatty acids • 1998 | View Paper
“Adding PGE1 to confluent cells maintained in its absence caused 71 +/- 17% (mean +/- SE, 10 experiments) inhibition of the conversion of retinol into retinoic acid.”
Archives of biochemistry and biophysics • 1993 | View Paper
“In contrast, in monolayers of PGE1‐independent MDCK cells, retinoic acid treatment resulted in an increase in dome frequency even in medium K‐1 lacking PGE1 This observation can be explained by the elevated cyclic adenosine monophosphate (cAMP) levels in these PGE1‐independent MDCK cells.”