Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.6.1.1 (adenylate cyclase)
19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine (HA), 1-1000 microM, significantly stimulated both basal and forskolin-activated cAMP generation in chicken and adult hen retina. The action of HA was reproduced by the selective H2-receptor agonists dimaprit and 4-methyl-histamine, but not by the selective H1-receptor agonist 2-thiazolylethylamine, and it was antagonized by the specific H2-receptor blockers cimetidine and tiotidine, but not by the H1-receptor blocker mepyramine. In parallel experiments, dopamine, an established retinal neuromodulator acting through the D1-type of receptor, also stimulated basal and forskolin-driven adenylate cyclase activity in homogenate of chicken retina. It is suggested that chicken retina contains HA H2-receptors which are positively coupled to the adenylate cyclase system.
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PMID:Cyclic AMP generating systems in vertebrate retina: effects of histamine and an established retinal modulator, dopamine. 168 Feb 73

The H2 subclass of histamine receptors mediates gastric acid secretion, and antagonists for this receptor have proven to be effective therapy for acid peptic disorders of the gastrointestinal tract. The physiological action of histamine has been shown to be mediated via a guanine nucleotide-binding protein linked to adenylate cyclase activation and cellular cAMP generation. We capitalized on the technique of polymerase chain reaction, using degenerate oligonucleotide primers based on the known homology between cellular receptors linked to guanine nucleotide-binding proteins to obtain a partial-length clone from canine gastric parietal cell cDNA. This clone was used to obtain a full-length receptor gene from a canine genomic library. Histamine increased in a dose-dependent manner cellular cAMP content in L cells permanently transfected with this gene, and preincubation of the cells with the H2-selective antagonist cimetidine shifted the dose-response curve to the right. Cimetidine inhibited the binding of the radiolabeled H2 receptor-selective ligand [methyl-3H]tiotidine to the transfected cells in a dose-dependent fashion, but the H1-selective antagonist diphenhydramine did not. These data indicate that we have cloned a gene that encodes the H2 subclass of histamine receptors.
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PMID:Molecular cloning of a gene encoding the histamine H2 receptor. 206 72

The effects of histamine on delayed K+ current (IK) were investigated in patch-clamped single guinea pig ventricular myocytes. Histamine increased IK with a maximal fractional response of 2.7 and a kd of 9.4 x 10(-7) mol/l. At a concentration of 10(-8) mol/l, histamine did not increase IK significantly, but increased ICa by 52% +/- 12%. The voltage-dependence of IK activation, the reversal potential and the time course of the IK tail decay were not changed by histamine. Under pretreatment with 10(-4) mol/l of ranitidine, neither histamine (10(-6) mol/l) nor 2-pyridylethylamine (10(-4) mol/l) caused any sizable increase in IK. When the cell was pretreated with a saturating dose of isoproterenol (10(-6) mol/l), histamine did not additively enhance IK. The IK enhancement by 3 x 10(-7) mol/l histamine was partially antagonized by concurrent exposure to 5 x 10(-6) mol/l carbachol. Whereas, use of a higher concentration of histamine (10(-6) mol/l) obscured the inhibitory effect of carbachol. It is concluded that histaminergic action of IK is attributed exclusively to H2 receptor-mediated reactions involving GS protein and adenylate cyclase.
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PMID:Modulation of the delayed K+ current by histamine in guinea pig ventricular myocytes. 181 Nov 75

In isolated and enriched guinea-pig gastric mucous cells the effects of carbachol, prostaglandin E2 (PG E2), prostaglandin F2 alpha (PG F2 alpha) and histamine on adenylate cyclase (AC) and cytosolic free Ca2+ were investigated, in order to study the biochemical mechanisms involved in secretagogue-mediated mucus release. Histamine and both prostaglandins stimulated AC in partially purified membranes of mucous cells. Histamine was most efficacious, followed by PG E2 and PG F2 alpha. The histamine effect was blocked by the H2-receptor antagonist ranitidine, but not by the H1-receptor antagonist mepyramine. Carbachol raised the resting [Ca2+]i in mucous cells from 120 to 306 nM. This carbachol effect was blocked by atropine. Histamine and PG E2 stimulation of AC was inhibited in a concentration-dependent manner by Ca2+ (IC50:31 microM). In the presence of TPA and phosphatidylserine, conditions which activate protein kinase C, the inhibitory action of Ca2+ on AC was significantly increased. These data indicate that there exists a negative feedback control mechanism between protein kinase C and histamine/prostaglandin E2-induced AC activation. From the finding that TPA and phosphatidylserine increased the inhibitory action of Ca2+ on cholera toxin-, but not on forskolin-stimulated AC we assume that the point, where protein kinase C exerts its inhibitory effect at the AC, is the guanine nucleotide regulatory protein.
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PMID:Signal transduction pathway in gastric mucous cells. 182 37

Intracellular Ca2+ ([Ca2+]i) is thought to act as a second messenger of transmembrane signalling systems. However, no measurement of [Ca2+]i has been made in intact epidermal keratinocytes. We have developed a method for measuring [Ca2+]i in human keratinocytes from pure epidermal sheet by the application of digital imaging fluorescence microscopy with the use of Fura 2-AM. Normal human pure epidermal sheets were obtained by dispase treatment. Epinephrine and salbutamol induced transient [Ca2+]i increases. Propranolol, a beta-antagonist, inhibited this response, while prazosin and yohimbine (alpha 1- and alpha 2-antagonists, respectively) did not affect the response. Histamine and adenosine, also receptor agonists of the epidermal adenylate cyclase system, induced a similar [Ca2+]i increase, as did forskolin, a direct activator of adenylate cyclase. These data coincide with those previously presented for cultured human epidermal keratinocytes, and reveal that adenylate cyclase activation induces an increase of [Ca2+]i in intact epidermal cells. This technique enables the kinetics of [Ca2+]i in various skin disorders to be investigated.
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PMID:Adenylate cyclase induces intracellular Ca2+ increase in single human epidermal keratinocytes of the epidermal sheet as measured by digital imaging microscopy using Fura 2-AM. 206 17

The present study examined the effect of histamine on the secretion of phosphatidylcholine, the predominant component of pulmonary surfactant from adult rat alveolar type II pneumocytes in primary culture. Histamine stimulated surfactant secretion in a time- and dose-dependent manner. At a concentration of 10 microM, histamine stimulated surfactant release by 5.2-fold over the basal secretory rate. The concentration producing half the maximal response for histamine-induced secretion was 70 nM. Histamine-induced secretion was blocked by both the selective histamine1 receptor antagonist pyrilamine and the selective histamine2 receptor antagonist cimetidine, but not by the beta-adrenergic antagonist alprenolol. Histamine activated adenylate cyclase and intracellular adenosine 3',5'-cyclic monophosphate (cAMP) production. These effects on adenylate cyclase and cAMP induced by histamine were inhibited by the H2 antagonist cimetidine. This would suggest that surfactant secretion was stimulated by histamine through H2 receptors and by cAMP. When histamine and isoproterenol were added concomitantly, the effects on phosphatidylcholine secretion were additive; however, there was no additive effect on adenylate cyclase activation. This coupled with H2 antagonist pyrilamine inhibition of histamine-induced secretion would suggest that histamine stimulated surfactant secretion through another mechanism in addition to a cAMP-dependent mechanism.
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PMID:Histamine stimulation of surfactant secretion from rat type II pneumocytes. 215 24

The adenylate cyclase system of FRSK cells, a cultured cell line of fetal rat epidermal keratinocytes, and SV40-transformed human keratinocytes was investigated. Stimulators of the human epidermal adenylate cyclase, epinephrine, adenosine, and prostaglandin E2 increased cyclic AMP levels of these cells. There were marked differences in the stimulatory effects; while epinephrine revealed a much stronger effect than the other stimulators in FRSK cells, epinephrine and prostaglandin E2 revealed similarly marked effects in SV40-transformed cells. Histamine had little or only slight effect on the cyclic AMP levels of these cells. Cholera toxin and forskolin, which work on the stimulatory guanine nucleotide binding protein (Gs) and the catalytic component of adenylate cyclase, respectively, also increased cyclic AMP levels. Northern blot hybridization analysis revealed that both FRSK cells and SV40-transformed human keratinocytes express mRNAs for the beta 2-adrenergic receptor, as well as the stimulatory and inhibitory guanine nucleotide binding proteins (Gs and Gi, respectively). The presence of Gs as well as Gi were confirmed by cholera toxin-, and pertussis toxin (IAP)-induced ADP-ribosylation of membranous proteins of these cells. Our results indicate that both FRSK cells and SV40-transformed human keratinocytes express the fundamental components of the adenylate cyclase system. These cell lines might be useful tools for the analysis of the adenylate cyclase system in epidermal keratinocytes.
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PMID:Adenylate cyclase system in fetal rat keratinizing epidermal cells (FRSK cells) and SV40-transformed human keratinocytes. 217 43

Histamine stimulated large increases of cyclic adenosine monophosphate (cAMP) in freshly isolated human blood monocytes in the presence of R02-1724, a specific cAMP phosphodiesterase inhibitor. This was mediated by H2 receptors, since it was inhibited by cimetidine but not chlorpheniramine. Stimulation was attenuated in cells aged in culture 1-2 days. Indomethacin prevented the desensitization, suggesting that a cyclooxygenase product was responsible. Desensitization was heterologous, since the adenylate cyclase responses to 5'-(N-ethylcarboxamido)adenosine (A2 receptor agonist), isoproterenol (beta-adrenoceptor agonist), and prostaglandin E2 (PGE2) also declined during culture. The loss of sensitivity to histamine was restored by incubating monocytes with PGE2 in the presence of indomethacin. The results indicate that, while PGE2 inhibits monocyte functions via cAMP, its accumulation paradoxically permits cells to escape this regulation through a heterologous desensitization of the cAMP response to itself and other agonists.
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PMID:Prostaglandin-dependent desensitization of human monocyte cAMP responses. 217 33

Hippocampal slices from rat brain were exposed to histamine and related substances in a perfusion chamber. Granule cells of the dentate gyrus were studied with conventional extra- and intracellular recording and a single electrode voltage clamp. Histamine caused, through activation of H(2)-receptors, a small depolarization, an increase in the number of synaptic and action potentials, a block of the long lasting (but not the early) component of spike afterhyperpolarizations and a reduction of the accommodation of action potential firing. These effects were mimicked by forskolin (suggests activation of adenylate cyclase). In voltage clamp, histamine blocked a long lasting calcium-dependent outward tail current without any reduction of inward current. Thus histamine selectively blocks the late calcium-dependent potassium current in dentate granule cells which receive histaminergic input from the posterior hypothalamus. Histamine also reduces the field excitatory postsynaptic potential evoked by perforant path stimulation. These actions allow for a powerful modulation of excitatory signals and an effective regulation of hippocampal excitability.
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PMID:Effects of histamine on dentate granule cells in vitro. 233 45

The H1-histamine receptor antagonist [3H]mepyramine bound with high affinity (Kd = 3-5 nM) to membranes derived from 1321N1 human astrocytoma cells. The H1-receptor antagonists triprolidine and diphenhydramine inhibited [3H]mepyramine binding with Kj values of 1-5 nM, whereas the Kj of the H2-histamine receptor antagonist cimetidine was greater than 100 microM. Histamine also inhibited [3H]mepyramine binding to 1321N1 cell membranes, and the histamine inhibition curve was shifted to the right and steepened in the presence of 1 microM guanosine 5'-O-(3-thiotriphosphate). Treatment of 1321N1 cells with pertussis toxin had no effect on the capacity of histamine to inhibit [3H]mepyramine binding either in the absence or presence of guanosine 5'-O-(3-thiotriphosphate). Therefore, agonist-occupied histamine receptors in these cells apparently interact with a guanine nucleotide regulatory protein that is not the inhibitory guanine nucleotide regulatory protein of adenylate cyclase. Although adenylate cyclase activity was not affected by histamine in a cell-free preparation, incubation of 1321N1 cells with histamine resulted in an attenuation of cyclic AMP accumulation. Analysis of cyclic AMP degradation in the presence of histamine indicated that the effects of histamine on cyclic AMP accumulation are mediated through activation of phosphodiesterase. This idea was supported by the fact that the phosphodiesterase inhibitor 1-isobutyl 3-methylxanthine blocked attenuation of cyclic AMP accumulation by histamine in a noncompetitive manner. Histamine also markedly increased phosphoinositide breakdown and 45Ca2+ efflux in 1321N1 cells. These histamine-induced effects apparently are mediated through H1-receptors, since triprolidine, but not cimetidine, potently inhibited histamine action. As for histamine interaction with its receptor, pertussis toxin had no effect on histamine-induced phosphoinositide breakdown, 45Ca2+ efflux, or attenuation of cyclic AMP accumulation. Taken together, these data indicate that 1321N1 human astrocytoma cells are a useful model system for the study of H1-histamine receptors and the biochemical responses mediated through these receptors.
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PMID:H1-histamine receptors on human astrocytoma cells. 241 44


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