Activation of PTGIR by incubation of LE and ST cells with iloprost resulted in greater cAMP generation (P < 0.01).
IMD affected cAMP generation in the myocardium and aorta, which were not attenuated by prior addition of either CGRP8 37 or ADM22 52 alone.
Treatment of T24 cells with 100 nM PGE2 resulted in a significant elevation in cAMP generation confirming the expression of functional PGE2 receptors.
Photoactivation of optoMOR decreased the Ca2+ influx and inhibited the forskolin-induced cAMP generation, activation of CREB, and BDNF levels in optoMOR-expressing cells similar to the activation of native μ-opioid receptor by DAMGO.
Peptoid 5 displaced both radiolabeled Nle4-α-MSH (IC50=3.1 μM) and AGRP (86 132) (IC50=1.9 μM) from the human melanocortin-4 receptor and functioned as an antagonist of α-MSH stimulated cAMP generation, thus providing an important lead in the development of AGRP mimetics.
Heterologous expression of the three major splice variants of the rat PAC1 receptor, PAC1hop, null and hip, in neural NG108-15 conferredferred PACAP-mediated intracellular cAMP generation, while elevation of [Ca2+]i occurred only in PAC1hop-, and to a lesser extent in PAC1null-expressing cells.
Treatment with an activator of adenylate cyclase, forskolin, or a cell-permeable analog of cAMP, 8-Br-cAMP, enhanced Ca2+-stimulated Fgf-2 expression, but a single treatment with forskolin or 8-Br-cAMP did not, suggesting that cAMP generation is indispensable but not sufficient for Ca2+-stimulated FGF2 expression.
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For dissociation studies and cAMP generation, bovine TSH was used (Sigma).
These responses to PGE2 are unusually robust and can result in dramatic morphological changes that are driven by cAMP generation.
Thus, transcriptional up-regulation of target genes resulting from cAMP generation relies on the formation of a CREB/CBP complex.
