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)

Starvation of Saccharomyces cerevisiae cells for specific nutrients such as nitrogen, phosphate or sulphate causes arrest in the G1 phase of the cell cycle at a specific point called 'start'. Re-addition of different nitrogen sources, phosphate or sulphate to such starved cells causes activation of trehalase within a few minutes. Nitrogen-source- and sulphate-induced activation of trehalase were not associated with any change in the cAMP level, but in the case of phosphate there was a small transient increase. When nitrogen-source-activated trehalase was isolated by immuno-affinity chromatography from crude extracts, the purified enzyme showed the same activity profile as in the original crude extracts, indicating that post-translational modification is responsible for the activation. In the yeast mutants cdc25-5 and cdc35-10, which are temperature sensitive for cAMP synthesis, incubation at the restrictive temperature lowered but did not prevent nitrogen-, phosphate- or sulphate-induced activation of trehalase. Since under these conditions the cAMP level in the cells is very low, it is unlikely that cAMP acts as a second messenger in this nutrient-induced effect. Nitrogen-source-induced activation of trehalase requires the presence of glucose at a concentration similar to that able to stimulate the RAS-adenylate cyclase pathway. This indicates that the same glucose-sensing system might be involved in both phenomena. Nitrogen-starved cells fractionated according to cell size all showed nitrogen-source-induced activation of trehalase to the same extent, indicating that the nitrogen-induced signalling pathway involved is not dependent on the well-known cell size requirement for progression over the start point of the cell cycle.
J Gen Microbiol 1992 Oct
PMID:Nutrient-induced activation of trehalase in nutrient-starved cells of the yeast Saccharomyces cerevisiae: cAMP is not involved as second messenger. 133 29

In homogenates of female rat anterior pituitary, the azepine derivative B-HT 920 inhibited the forskolin-stimulated adenylate cyclase activity with an EC50 value of 0.35 microM. In male rat anterior pituitary, B-HT 920 curtailed the stimulation of adenylate cyclase activity by vasoactive intestinal peptide with an EC50 of 0.20 microM. In synaptic plasma membranes of rat striatum, B-HT 920 significantly reduced basal adenylate cyclase activity with an EC50 of 0.68 microM. Both in pituitary and striatum, the B-HT 920 inhibition was counteracted by the dopamine (DA) D2 receptor antagonist 1-sulpiride, but not by the alpha 2-adrenergic antagonist yohimbine. These results indicate that B-HT 920 is capable of activating DA D2 receptors negatively coupled to adenylate cyclase activity.
J Neural Transm Gen Sect 1992
PMID:B-HT 920 activates dopamine D2 receptors coupled to inhibition of adenylate cyclase activity. 135 80

1. Decreased beta-adrenergic and serotonergic responses have been reported in gastro-intestinal tract of experimentally diabetic rats. Effects of lithium on the decreased beta-adrenergic and serotonergic responsiveness of the gastro-intestinal tract due to diabetes were investigated using gastric fundus strips and proximal duodenum from alloxan diabetic rats. 2. A 6-day treatment with lithium chloride (2 mEq/kg i.p. in saline) normalized the decreased gastro-intestinal responses of the alloxan-diabetic rats, whereas the lithium treatment did not affect the elevated blood glucose levels due to experimental diabetes. 3. Furthermore, the lithium treatments of control and alloxan-diabetic rats did not alter the relaxing effect of manganese chloride on the isolated duodenum. 4. These results strongly suggest that the improving effect of lithium is not related to adenylate cyclase activation and may be as a consequence of its direct action on the diabetic gastro-intestinal smooth muscles.
Gen Pharmacol 1992 Jul
PMID:Effect of lithium on gastro-intestinal complications in alloxan-diabetic rats. 139 84

In the mantle of the female sea mussel Mytilus galloprovincialis seasonal variations in the adenylate cyclase activity correlate with gonadal development. Two peaks of adenylate cyclase activity were found in spring and autumn, both periods of gonadal development. The lowest enzymatic activities were in summer, a gonadal resting period.
Gen Comp Endocrinol 1992 May
PMID:Pattern of the mantle adenylate cyclase activity during the reproductive cycle of the female Mytilus galloprovincialis. 160 Dec 66

As part of a study of the effects of lithium carbonate on neurochemical function in man, platelet and lymphocyte adenylate cyclase activity and lymphocyte beta-adrenergic receptor binding characteristics were determined before and after 2 weeks of lithium treatment in 10 normal volunteers. Lithium had differential effects on platelet and lymphocyte adenylate cyclase activity. In platelets, basal and stimulated (guanyl imidodiphosphate [Gpp[NH]p] or cesium fluoride) adenylate cyclase activity was significantly augmented by lithium treatment. By contrast, in lymphocytes, Gpp(NH)p- and cesium fluoride-stimulated adenylate cyclase activity was unaffected, while basal activity was decreased modestly after lithium. These results are consistent with preclinical studies that suggest that lithium's effects on adenylate cyclase activity are specific with respect to tissue and brain region and that lithium may interfere with guanine nucleotide binding (G) protein function. Lithium treatment significantly increased the ratio of low- to high-affinity dissociation constants for agonist displacement of antagonist binding to lymphocyte beta-adrenergic receptors (thought to reflect coupling between the beta-adrenergic receptor and stimulatory G protein). Lithium had significant effects on measures associated with signal transduction that might be contrasted to its more subtle effects on neuronal function (norepinephrine release) and neuroendocrine systems (responses to serotoninergic challenge) in these same subjects (reported in a companion article). Lithium's primary site of action may be on signal transduction mechanisms. These effects subsequently may be manifested in changes in neurotransmitter function that may be important to lithium's mood-stabilizing actions.
Arch Gen Psychiatry 1991 Jun
PMID:The mechanisms of action of lithium. II. Effects on adenylate cyclase activity and beta-adrenergic receptor binding in normal subjects. 164 14

Hormonal modulation of neurotransmission emerged as a concept from the recognition that adrenocortical steroids exert profound effects at the level of receptors, G-proteins and effector units. G-proteins, a family of guanine nucleotide binding regulatory components that couple neurotransmitter receptors to various types of intracellular effector systems, appear to be a key target of glucocorticoid (GC) action in the CNS. It is thought that Gs/Gi mediates stimulation/inhibition of adenylate cyclase (AC system), which forms cyclic AMP as second messenger, while receptors stimulating phospholipase C do so through Go to produce two second messengers, inositol 1,4,5-triphosphate and diacylglycerol (PI system). Recent evidence suggests that GC increase Gs alpha-and decrease Gi alpha-protein subunit expression without affecting Go alpha. Activation of central pre- and postsynaptic 5-HT1A receptors which are linked to the Gi-AC complex, induces hypothermia and ACTH/cortisol release in rodents and humans. Compared with controls, patients with a major depressive disorder exhibit increased basal cortisol secretion associated with decreased hypothermic and ACTH/cortisol responses. The attenuated neuroendocrine and thermoregulatory response to 5-HT1A receptor activation may reflect a GC-dependent feedback inhibition of the hypothalamic-pituitary-adrenal (HPA) system and subsensitivity of the presynaptic 5-HT1A-Gi-AC complex function. Differential regulation of 5-HT1A and 5-HT2 function leading to a relative 5-HT2-Go-PI complex supersensitivity may maintain HPA hyperactivity during the course of depression. These findings corroborate recent reports that GC, via GC-GC receptor (GR) complex activated promotion of gene transcription, modify the expression 5-HT1A-coupled Gi (but not 5-HT2-coupled Go) resulting in altered sensitivity of 5-HT1A-mediated signal transduction and further support the hypothesis of a differential regulation of 5-HT1A and 5-HT2 receptor function and a GC-GR/5-HT1A-G-protein--effector system-related abnormality in depression.
J Neural Transm Gen Sect 1991
PMID:The 5-HT receptor--G-protein--effector system complex in depression. I. Effect of glucocorticoids. 164 69

Cytochalasin B (CB) and the more specific cytochalasin D (CD), disruptors of microfilament polymerization, and colchicine, an inhibitor of microtubule polymerization, were studied for their effects on cAMP and steroid production in granulosa cells of domestic fowl. Each agent was incubated with freshly dispersed cells from the largest preovulatory follicle of laying hens taken 3-4 hr before expected ovulation. Total content (cells + medium) of cAMP and steroids was measured by established radioimmunoassays. CB dose dependently inhibited basal as well as LH- and forskolin-stimulated cAMP generation and diminished basal, LH- and 25-hydroxycholesterol (25-OHC)-supported progesterone production. Conversely, CD potentiated LH- and forskolin-promoted cAMP generation as well as LH- and 25-OHC-stimulated progesterone synthesis. Neither drug had any influence on metabolism of pregnenolone to progesterone. Colchicine had no effect on cyclic AMP generation, yet it suppressed progesterone synthesis by inhibiting the conversion of pregnenolone to progesterone. beta-Lumicolchicine, a colchicine analog that does not depolymerize microtubules, had no such effect. The results suggest that microfilaments are involved in steroidogenesis at two sites, namely, the adenylate cyclase-cAMP system, and cholesterol conversion to pregnenolone; whereas microtubules act on the conversion of pregnenolone to progesterone.
Gen Comp Endocrinol 1991 Jun
PMID:Participation of the cytoskeleton in avian granulosa cell steroidogenesis. 165 30

The electrophysiological effects of three selective D1 dopamine (DA) receptor agonists, which exhibit different potencies and efficacies for stimulation of adenylate cyclase, were compared in the rat nucleus accumbens (NAc) using single unit recording and microiontophoretic techniques. The partial agonists SKF75670 and SKF38393, and the full agonist SKF81297 produced nearly identical current-response curves for the inhibition of firing of NAc neurons. In rats acutely depleted of DA by alpha-methyl-p-tyrosine (AMPT) pretreatment, all three D1 agonists enabled the inhibition of firing produced by the selective D2 receptor agonist quinpirole, with SKF38393 exerting the greatest efficacy, followed by SKF81297 and SKF75670. Thus, no apparent relationship was found between the previously reported ability of these compounds to stimulate cyclic adenosine monophosphate (cAMP) production and their ability either to inhibit the firing of NAc neurons or to enable quinpirole-mediated inhibition of firing in DA-depleted rats. In addition, the membrane-permeable cAMP analog 8-bromo-cAMP also caused a current-dependent inhibition of the firing of NAc neurons, but failed to enable quinpirole-mediated inhibition in AMPT-pretreated animals. These results suggest either that only a small percentage of D1 receptors need to be stimulated to produce these electrophysiological effects, or that D1 receptors exist within the rat NAc which are linked to transduction mechanisms other than, or in addition to, adenylate cyclase.
J Neural Transm Gen Sect 1991
PMID:Relationship between D1 dopamine receptors, adenylate cyclase, and the electrophysiological responses of rat nucleus accumbens neurons. 168 41

Accumulation or inhibition of cAMP formation in response to dopamine or dopamine related drugs in the absence or in the presence of forskolin and/or IBMX was investigated in isolated rat retina. While the existence of D1-receptors (positively coupled with adenylate cyclase) was confirmed, D2-receptors (negatively coupled to adenylate cyclase) were also revealed by using a selective D1-antagonist (SCH 23390), a D2-agonist (LY 171555) or two D2-antagonists (S-sulpiride, spiroperidol). These results indicate that rat retina may be used for the study of both types of dopamine-receptors.
J Neural Transm Gen Sect 1990
PMID:Bidirectional regulation of cAMP generating system by dopamine-D1 and D2-receptors in the rat retina. 169 54

Altered osmotic pressure and somatostatin (SRIF) rapidly alter prolactin (PRL) release from the pituitary gland of the euryhaline teleost, the tilapia. The present studies were undertaken to determine whether altered osmotic pressure and SRIF influence cAMP metabolism in a manner that is correlated with the pattern of PRL release observed previously. Although PRL release is stimulated within 10-20 min when medium osmotic pressure is reduced, cAMP metabolism was not altered. However, following 1 hr of incubation in the presence of IBMX, cAMP accumulation was higher in PRL tissue exposed to medium of reduced osmotic pressure. This suggests that cAMP does not initiate an increase in PRL release in response to reduced osmotic pressure. By contrast, SRIF reduced the forskolin-stimulated increase in cAMP levels in a manner consistent with its rapid effects on PRL release. Moreover, the ability of SRIF to suppress the forskolin-stimulated increase in cAMP levels suggests that SRIF may act to render adenylate cyclase less responsive to direct stimulation by forskolin.
Gen Comp Endocrinol 1991 Jul
PMID:Effects of osmotic pressure and somatostatin on the cAMP messenger system of the osmosensitive prolactin cell of a teleost fish, the tilapia (Oreochromis mossambicus). 171 2


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