Inhibitory actions of dopamine on Limulus visceral muscle involve a cyclic AMP-dependent mechanism

1992 ◽  
Vol 170 (6) ◽  
Author(s):  
JamesR. Groome ◽  
CharlesM. Lent
Keyword(s):  
Cyclic Amp ◽  
Visceral Muscle ◽  
Dependent Mechanism

Activation of human platelets by 2-arachidonoylglycerol is enhanced by serotonin

2003 ◽  
Vol 89 (02) ◽  
pp. 340-347 ◽  
Author(s):  
Monica Bari ◽  
Domenico Del Principe ◽  
Alessandro Finazzi-Agrò ◽  
Mauro Maccarrone
Keyword(s):  
Cyclic Amp ◽  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Platelet Rich Plasma ◽  
Maximum Velocity ◽  
Human Platelets ◽  
Platelet Surface ◽  
Therapeutic Implications ◽  
Inositol 1,4,5 Trisphosphate ◽  
Dependent Mechanism

SummaryThe endocannabinoid 2-arachidonoylglycerol (2-AG) has been shown to activate human platelets in platelet-rich plasma, by binding to a “platelet-type” cannabinoid receptor (CBPT). Here, washed human platelets were used to characterize the binding of [3H]2-AG to CBPT, showing a dissociation constant (Kd) of 140 ± 31 nM and a maximum binding (Bmax) of 122 ± 10 pmol.mg protein-1. Selective antagonists of both CB1 and CB2 cannabinoid receptors inhibited this binding, which was enhanced up to ~230% over the controls by 1 µM serotonin (5-hydroxytryptamine, 5-HT). Human platelets were also able to bind [3H]5-HT (Kd = 79 ± 17 nM, Bmax = 14.6 ± 1.3 pmol.mg protein-1), and 1 µM 2-AG enhanced this binding up to ~150%. Moreover, they were able to take up [3H]5-HT through a high affinity transporter (Michaelis-Menten constant = 22 ± 2 nM, maximum velocity = 344 ± 15 pmol.min-1.mg protein-1), which was not affected by 2-AG. Interestingly, 5-HT did not affect the activity of the 2-AG transporter of human platelets. Treatment of washed platelets with 1 µM 2-AG led to increased intracellular inositol-1,4,5-trisphosphate (up to ~300%) and decreased cyclic AMP (down to ~50%). Furthermore, treatment of pre-loaded platelets with 1 µM 2-AG induced a ~300% increase in [3H]2-AG release, according to a CBPT-dependent mechanism. Also, 1 µM 5-HT enhanced the effect of 2-AG on inositol-1,4,5-trisphosphate (~500% of the controls), cyclic AMP (~20%) and [3H]2-AG release (~570%), and the latter process was shown to be partly (~50%) involved in the 5-HT-dependent platelet activation. Taken together, reported findings represent the first demonstration that 2-AG and 5-HT can mutually reinforce their receptor binding on platelet surface, which might have therapeutic implications.

Modulating a modulator: biogenic amines at subthreshold levels potentiate peptide-mediated cardioexcitation of the heart of the tobacco hawkmoth Manduca sexta.

1994 ◽  
Vol 197 (1) ◽  
pp. 377-391 ◽  
Author(s):  
K R Prier ◽  
O H Beckman ◽  
N J Tublitz
Keyword(s):  
Cyclic Amp ◽  
Manduca Sexta ◽  
Biogenic Amine ◽  
Molecular Mechanisms ◽  
Adult Heart ◽  
The Central Nervous System ◽  
Messenger System ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Dependent Mechanism

The central nervous system of the moth Manduca sexta contains a group of myoregulatory neuropeptides, the CAPs (Cardioacceleratory Peptides), which cause a physiologically important, dose-dependent increase in heart rate during wing inflation and flight in adult moths. We report here that the response of the adult heart to a subset of the CAPs, the CAP2S, is potentiated nearly twofold in the chronic presence of subthreshold levels of the biogenic amine octopamine or near-threshold levels of the biogenic amine serotonin. Subthreshold levels of the CAP2S fail to alter the response of the heart to octopamine. We have begun to investigate the molecular mechanisms underlying this potentiation. Previous work on the adult heart has shown that the CAP2s act through an inositol-1,4,5-trisphosphate second-messenger system. Here, we demonstrate that the cardioexcitatory effects of the two amines, in contrast to those of the CAP2S, are both mediated by cyclic AMP. Application to the heart of either 10(-5) moll-1 octopamine or 10(-6)moll-1 serotonin elicits a threefold increase in intracellular cyclic AMP levels. The CAP2S have no effect on cyclic AMP levels in the heart. These results illustrate a mechanism by which the effectiveness of a neurohormone can be increased with minimal cost to the animal. In Manduca sexta, subthreshold levels of octopamine are found in the haemolymph during wing inflation and flight. Thus, it is possible that octopamine up-regulates the effects of CAP2 via a cyclic-AMP-dependent mechanism during these activities.

A cyclic AMP protein kinase A-dependent mechanism by which rotavirus impairs the expression and enzyme activity of brush border-associated sucrase-isomaltase in differentiated intestinal Caco-2 cells

2004 ◽  
Vol 6 (8) ◽  
pp. 719-731 ◽  
Author(s):  
Sandra Martin-Latil ◽  
Jacqueline Cotte-Laffitte ◽  
Isabelle Beau ◽  
Anne-Marie Quéro ◽  
Monique Géniteau-Legendre ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Protein Kinase A ◽  
Brush Border ◽  
Kinase A ◽  
Dependent Mechanism

scholarly journals The Phosphorylation Status of a Cyclic AMP-Responsive Activator Is Modulated via a Chromatin-Dependent Mechanism

2000 ◽  
Vol 20 (5) ◽  
pp. 1596-1603 ◽  
Author(s):  
Laura F. Michael ◽  
Hiroshi Asahara ◽  
Andrew I. Shulman ◽  
W. Lee Kraus ◽  
Marc Montminy
Keyword(s):  
Cyclic Amp ◽  
Target Gene ◽  
Regulatory Mechanism ◽  
Gene Activation ◽  
Hdac Inhibitors ◽  
Histone Acetyltransferases ◽  
Creb Binding Protein ◽  
Creb Phosphorylation ◽  
P300 Recruitment ◽  
Dependent Mechanism

ABSTRACT Cyclic AMP (cAMP) stimulates the expression of numerous genes via the protein kinase A (PKA)-mediated phosphorylation of CREB at Ser133. Ser133 phosphorylation, in turn, promotes recruitment of the coactivator CREB binding protein and its paralog p300, histone acetyltransferases (HATs) that have been proposed to mediate target gene activation, in part, by destabilizing promoter bound nucleosomes and thereby allowing assembly of the transcriptional apparatus. Here we show that although histone deacetylase (HDAC) inhibitors potentiate target gene activation via cAMP, they do not stimulate transcription over the early burst phase, during which CREB phosphorylation and CBP/p300 recruitment are maximal. Rather, HDAC inhibitors augment CREB activity during the late attenuation phase by prolonging CREB phosphorylation on chromosomal but, remarkably, not on extrachromosomal templates. In reconstitution studies, assembly of periodic nucleosomal arrays on a cAMP-responsive promoter template potently inhibited CREB phosphorylation by PKA, and acetylation of these template-bound nucleosomes by p300 partially rescued CREB phosphorylation by PKA. Our results suggest a novel regulatory mechanism by which cellular HATs and HDACs modulate the phosphorylation status of nuclear activators in response to cellular signals.

CONTROL OF DRUG-INDUCED ENZYMES BY A CYCLIC AMP-DEPENDENT MECHANISM

Abstracts ◽  
1977 ◽  
pp. 254
Author(s):  
Diane H. Russel ◽  
Craig V. Byus ◽  
Max Costa ◽  
I. Glenn Sipes ◽  
Bernard B. Brodie
Keyword(s):  
Cyclic Amp ◽  
Drug Induced ◽  
Dependent Mechanism

scholarly journals Exchange Protein Directly Activated by Cyclic AMP Increases Melanoma Cell Migration by a Ca2+-Dependent Mechanism

2010 ◽  
Vol 70 (13) ◽  
pp. 5607-5617 ◽  
Author(s):  
Erdene Baljinnyam ◽  
Mariana S. De Lorenzo ◽  
Lai-Hua Xie ◽  
Mizuka Iwatsubo ◽  
Suzie Chen ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cyclic Amp ◽  
Melanoma Cell ◽  
Dependent Mechanism ◽  
Exchange Protein

Thrombin inhibits proliferation of the human megakaryoblastic MEG-01 cell line: A possible involvement of a cyclic-AMP dependent mechanism

1992 ◽  
Vol 150 (1) ◽  
pp. 65-75 ◽  
Author(s):  
Daniel Vittet ◽  
Marie-No�lle Mathieu ◽  
Jean-Marie Launay ◽  
Claude Chevillard
Keyword(s):  
Cyclic Amp ◽  
Cell Line ◽  
Dependent Mechanism
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