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)

Cyclic AMP (cAMP) in blood samples was followed during abortions induced with an intraamniotic injection of prostaglandin F2a (PGF2a) and E2 (PGE2) in women in the second trimester. The effect of intraamniotic administration of PGE2 on tissue cAMP levels and adenyl cyclase (AC) and cyclic nucleotide phosphodiesterase (PDE) in myometrium, maternal abdominal rectus muscle, placenta, and fetal liver and leg muscle was studied in women undergoing abortion with hysterotomy. Saline was injected intraamniotically into controls. Plasma cAMP values showed inconsistent variation after injection of both types of PGs. On administration of PGE2 uterine contraction started after 3 minutes. Myometrial cAMP increased 4-fold within 10 minutes, and these values also showed inconsistent variation. Neither AC or PDE activities were affected in myometrium by PGE2.
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PMID:Cyclic adenosine 3',5'-monophosphate in prostaglandin-induced abortion. 437 12

The interaction between forskolin and vasoactive intestinal polypeptide (VIP) in the regulation of cyclic AMP production in GH3 pituitary tumour cells was investigated. Both forskolin (10nM-10 microns) and VIP (10pM-10nM) increased the cyclic AMP content of GH3 cells. Forskolin (50-100nM) was additive with VIP in stimulating cyclic AMP accumulation when low concentrations (less than 1 nM) of the peptide were used, but exhibited a synergistic interaction with higher VIP concentrations (10-100 nM). These effects on cyclic AMP accumulation were reflected in a leftward shift in the concentration-response curve for VIP-stimulated prolactin release from GH3 cells, a process known to be regulated by intracellular cyclic AMP concentrations. The synergy observed did not appear to be related to changes in cyclic nucleotide phosphodiesterase activity, since it was even more marked in the presence of isobutylmethylxanthine, a phosphodiesterase inhibitor. Studies of the time-course of VIP-induced changes in GH3-cell cyclic AMP content revealed that, with high concentrations of VIP, production ceased within 2 min of addition. This attenuation of cyclic AMP synthesis was still observed in the presence of isobutylmethylxanthine, but was markedly inhibited by low concentrations of forskolin (50-100nM). The results suggest that VIP-induced cyclic AMP production rapidly becomes desensitized. This process, which is prevented by forskolin, may be related to changes in the ability of the guanine nucleotide regulatory protein to couple receptor occupancy to activation of adenylate cyclase.
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PMID:Vasoactive-intestinal-polypeptide-stimulated adenosine 3',5'-cyclic monophosphate accumulation in GH3 pituitary tumour cells. Reversal of desensitization by forskolin. 608 46

Primary cultures of bovine adrenal medullary chromaffin cells were used to study the regulation of opioid peptide (OP) synthesis. Chromaffin cells continuously exposed to tetrabenazine, a drug that depletes cellular catecholamine stores, increase their OP contents between 32 hr and 6 days of treatment. At no time following tetrabenazine addition were increases in opiate receptor-inactive enkephalin-containing peptides (IECPs) observed. Because IECPs may serve as precursors to OPs, these results suggest increased processing of OP precursors following treatment with catecholamine-depleting drugs in addition to an increased rate of OP precursor synthesis. The increases in cellular OP levels induced by tetrabenazine were approximately proportional to the depletion in cellular catecholamines produced by this drug. Also, the effects of tetrabenazine on chromaffin cell OP and IECP contents were mimicked by inhibitors of catecholamine biosynthesis and other agents that decreased catecholamine stores, but not by supplementing the culture medium with catecholamines or catecholamine receptor agonists. Addition of 8-bromo-cAMP or forskolin, an activator of adenylate cyclase, to chromaffin cell cultures increased both OP and IECP stores. Inhibitors of cyclic nucleotide phosphodiesterase also increase chromaffin cell OP and IECP contents, although it is unclear whether these increases result from increased cyclic nucleotide levels. Hence, both alterations in some intracellular catecholamine pool and elevations of cAMP levels may trigger increases in the synthesis and processing of OPs and IECPs in the adrenal medullary chromaffin cell.
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PMID:Regulation of opioid peptide synthesis and processing in adrenal chromaffin cells by catecholamines and cyclic adenosine 3':5'-monophosphate. 609 47

PC12 cells, derived from a rat pheochromocytoma, were mutagenized and selected in media containing agents known to elevate intracellular concentrations of cyclic AMP (cAMP). More than 40 clones were isolated by selection with cholera toxin or 2-chloroadenosine or both. The variants that were deficient in accumulating cAMP were obtained by using a protocol in which 1 microM 8-bromo-cAMP was included in addition to the agonist. Certain of these variants were partially characterized with respect to the site of altered cAMP metabolism. The profiles of adenylate cyclase activity responsiveness of certain variants to guanosine-5'-(beta, gamma-imido) triphosphate and to forskolin resembled those of UNC and cyc phenotypes of S49 lymphoma cells, which are functionally deficient in the GTP-sensitive coupling protein, Ns. Other variants were characterized by increased cyclic nucleotide phosphodiesterase activity at low substrate concentration. Diverse morphological traits were observed among the variants, but it was not possible to assign them to a particular cAMP phenotype. Two revertants of a PC12 mutant were isolated and observed to have regained a cellular cAMP response to 2-chloroadenosine and to forskolin. It is hoped that these PC12 mutants will have utility for defining cAMP-mediated functions, including any links to the action of nerve growth factor, in cells derived from the neural crest.
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PMID:Mutants of PC12 cells with altered cyclic AMP responses. 609 39

A method is described for stimulation of cAMP levels in brain by direct injection of dopamine (DA) and other neuroactive substances. Intracerebral microinjection was preceded by intraperitoneal injection of 3-isobutyl-1-methylxanthine (IBMX) to inhibit cyclic nucleotide phosphodiesterase. In vivo adenylate cyclase and phosphodiesterase activities were terminated by focused microwave radiation and the injected tissue assayed for protein and cAMP content. Increases in cAMP levels in response to injections of DA were both time- and dose-dependent. Animals receiving only vehicle or sham injections into the olfactory tubercle had basal cAMP levels of 5 pmol/mg protein. Up to five-fold increases above basal (25 pmol cAMP/mg protein) were observed for DA. With the injection of other neuroactive substances, values ranging from 160 pmol cAMP/mg protein for norepinephrine (NE), to 15 pmol cAMP/mg protein for gamma-amino butyric acid (GABA) were observed. The present study demonstrates that neuroactive substances can stimulate cAMP production in vivo when injected directly into brain tissue.
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PMID:A method for stimulation of cyclic AMP levels in vivo by intracerebral injection in the rat olfactory tubercle. 609 56

In this study it was found that several agents which elevate cAMP levels in cells also increase dramatically the quantity of transmitter released from crayfish excitatory nerve terminals in response to a stimulus. With respect to time course and magnitude, the increase produced by one of these agents, the cyclic nucleotide phosphodiesterase inhibitor Squibb 20,009 (SQ 20,009), is unlike any reported for such a drug at a synapse. Additionally, SQ 20,009 potentiated the facilitation of transmitter release produced by serotonin (5-HT) at this synapse. These results establish a possible role for cAMP in the control and modulation of transmitter release at the crayfish neuromuscular junction (NMJ). They further suggest that 5-HT functions here by activation of a presynaptically located adenylate cyclase.
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PMID:Cyclic AMP, 5-HT, and the modulation of transmitter release at the crayfish neuromuscular junction. 611 88

The intracellular localization of adenylate cyclase and 3',5'-cyclic nucleotide phosphodiesterase in buffalo sperm was examined. Adenylate cyclase activity is distributed in heads (8.4%), midpieces (16.6%), tails (49.5%) and 5.7% in the soluble supernatant; the total recovery being 81%. A 4-fold increase in specific activity was observed in the tail fraction relative to sonicated suspension. Further fractionation of the tail fraction into plasma membrane and microtubules by dialysis against low ionic strength buffer was followed by marker enzymes (Mg2+ -ATPase, 5'-nucleotidase and alkaline phosphatase) as well as by examination of fractions under electron microscope. The recovered adenylate cyclase (79%) was found in microtubules (45%) and plasma membrane (34%). Cyclic nucleotide phosphodiesterase in tails was distributed in tail plasma membrane (13.7%), microtubules (31.5%) and cytosol (34%) with a total recovery of 80%. Similar results were obtained when the distribution of adenylate cyclase and cyclic nucleotide phosphodiesterase was studied by treatment with Triton X-100; 40% activity of adenylate cyclase present in tails (about 20% relative to sperm sonicate) appeared in the soluble form by this method. The results are discussed in relation to control of cyclic AMP levels in buffalo sperm by adenylate cyclase and cyclic nucleotide phosphodiesterase.
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PMID:Subcellular localization of adenylate cyclase of buffalo spermatozoa. 612 19

Clofibrate is a hypolipidemic agent that causes muscle protein breakdown in rats, and an acute muscular syndrome in man. It also inhibits adenylate cyclase in fat tissue. Muscle protein metabolism has been shown to be regulated by cyclic nucleotides. In the present experiments were measured several parameters of cyclic nucleotide metabolism to determine the role that cyclic nucleotides play in clofibrate-induced muscle protein degradation. It was found that clofibrate treatment did not alter cyclic nucleotide levels, nor did it change the activities of basal or hormone-stimulated adenylate cyclase, or cyclic nucleotide phosphodiesterase in muscle. Our results suggest that muscle protein breakdown in clofibrate-treated rats is not regulated by cyclic nucleotides.
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PMID:Clofibrate does not alter cyclic nucleotide metabolism in muscle. 613 74

The adenylate cyclase activity of membranes of Xenopus laevis oocytes and follicle cells was affected by the presence of 2-chloro-10-(3-aminopropyl)phenothiazine (CAPP) and two other antipsychotic drugs, fluphenazine and penfluridol. CAPP, at concentrations of 10 and 100 microM, had opposite effects on the activation of the oocyte adenylate cyclase by effectors that act through the G/F regulatory subunit. Under these conditions, the drug stimulated the activation by fluoride and drastically inhibited the activation by guanyl-5'-yl-imidodiphosphate [Gpp(NH)p] and by cholera toxin and GTP. The activity of the catalytic subunit measured in the presence of either Mn2+ or forskolin was not affected by 100 microM CAPP. however, concentrations of this drug above 100 microM inhibited the adenylate cyclase activated by fluoride or by forskolin and also inhibited the activity of a calmodulin-independent cyclic nucleotide phosphodiesterase present in the same oocyte membrane preparation. Oocyte adenylate cyclase has been shown previously to be inhibited by the hormone progesterone. The inhibitory effect of CAPP is additive to that measured with the hormone, indicating that these compounds act through different mechanisms. CAPP did not modify the concentration of Gpp(NH)p required to yield half-maximal activation and, although the drug inhibited more strongly at lower concentrations of Gpp(NH)p, saturating amounts of the guanine nucleotide did not reverse completely the inhibition caused by CAPP. The effects of these antipsychotic drugs on oocyte adenylate cyclase did not require the presence of free Ca2+ and were not altered by the addition of exogenous calmodulin and calcium.
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PMID:Inhibition by phenothiazine derivatives of the adenylate cyclase of amphibian oocytes. 613 13

An elevation of the intracellular cAMP concentration in C6 cells by cholera toxin or the cyclic nucleotide phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine causes a densitization of the beta-adrenergic-receptor-dependent synthesis of adenosine 3',5'-monophosphate. The specific binding of [3H]dihydroalprenolol to the beta-adrenergic receptors and the activation of the adenylate cyclase in vitro by fluoride anions and guanyl imidotriphosphate remain unchanged. It is likely that the desensitization is caused by an inhibition of beta-receptor coupling to the GTP-binding coupling protein in the adenylate cyclase complex. Furthermore, these experiments provide evidence that the loss of beta-receptor binding observed after incubation of cells with catecholamines is not a necessary consequence of the densensitization of receptor coupling dependent on adenosine 3',5'-monophosphate.
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PMID:A hormone-independent rise of adenosine 3',5'-monophosphate desensitizes coupling of beta-adrenergic receptors to adenylate cyclase in rat glioma C6-cells. 615 29


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