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)

Addition of glucose or related fermentable sugars to derepressed cells of the yeast Saccharomyces cerevisiae triggers a RAS-protein-mediated cAMP signal, which induces a protein phosphorylation cascade. Yeast strains without a functional CDC25 gene were deficient in basal cAMP synthesis and in the glucose-induced cAMP signal. Addition of dinitrophenol, which in wild-type strains strongly stimulates in vivo cAMP synthesis by lowering intracellular pH, did not enhance the cAMP level. cdc25 disruption mutants, in which the basal cAMP level was restored by the RAS2val19 oncogene or by disruption of the gene (PDE2) coding for the high-affinity phosphodiesterase, were still deficient in the glucose- and acidification-induced cAMP responses. These results indicate that the CDC25 gene product is required not only for basal cAMP synthesis in yeast but also for specific activation of cAMP synthesis by the signal transmission pathway leading from glucose to adenyl cyclase. They also show that intracellular acidification stimulates the pathway at or upstream of the CDC25 protein. When shifted to the restrictive temperature, cells with the temperature sensitive cdc25-5 mutation lost their cAMP content within a few minutes. After prolonged incubation at the restrictive temperature, cells with this mutation, and also those with the temperature sensitive cdc25-1 mutation, arrested at the 'start' point (in G1) of the cell cycle, and subsequently accumulated in the resting state G0. In contrast with cdc25-5 cells, however, the cAMP level did not decrease and normal glucose- and acidification-induced cAMP responses were observed when cdc25-1 cells were shifted to the restrictive temperature.(ABSTRACT TRUNCATED AT 250 WORDS)
J Gen Microbiol 1991 Feb
PMID:Involvement of the CDC25 gene product in the signal transmission pathway of the glucose-induced RAS-mediated cAMP signal in the yeast Saccharomyces cerevisiae. 184 65

The putative roles of different signal transduction pathways in the regulation of testicular androgen production in goldfish were investigated. In addition to the role of the gonadotropin-adenylate cyclase pathway, which was studied using human chorionic gonadotropin and forskolin, we determined the effects of changes in intracellular calcium content and protein kinase C activation on androgen production using calcium ionophore A23187 and phorbol 12-myristate 13-acetate (PMA), respectively. Testis fragments incubated in vitro respond to hCG in a time- and dose-dependent manner with a resultant increase in the secretion of testosterone (T) and 11-ketotestosterone (11-KT). Although ineffective alone, PMA (400 nM) and A23187 (4000 nM) stimulate a small but significant increase (3-fold above basal) in T production. This response is minor compared to the up to 200-fold increase in T secretion observed in response to either hCG or forskolin. PMA (25-400 nM) alone and A23187 (250-4000 nM) alone inhibit the stimulatory actions of hCG on T production. Unlike PMA, the inactive phorbol 4 alpha-phorbol didecanoate, which does not activate PKC, had no effect on hCG-stimulated T production. PMA and A23187 did not influence the effects of forskolin on T production, suggesting that the compounds exert their effects prior to adenylate cyclase activation. In summary, the present studies suggest that in addition to the stimulatory actions of the adenylate cyclase second messenger system, changes in intracellular calcium content and protein kinase C activation may modulate testicular androgen production in the goldfish.
Gen Comp Endocrinol 1991 Sep
PMID:The control of testicular androgen production in the goldfish: effects of activators of different intracellular signalling pathways. 193 14

In order to determine the relevance of 5-HT1A-related signal transduction in the mode of action of lithium and antidepressants, the effects of long-term treatment with these drugs on the 5-HT1A-mediated inhibition of forskolin-stimulated adenylate cyclase activity were investigated in the rat hippocampal membranes. Chronic administration of antidepressants altered neither the [3H]8-hydroxy-2-(di-n-propylamino)tetralin [( 3H]8-OH-DPAT) binding sites nor the inhibition of forskolin-stimulated adenylate cyclase activity by 5-HT. Long-term treatment with lithium did not affect the inhibitory effect of 5-HT on the forskolin-stimulated adenylate cyclase activity, either. Neither the stimulation by forskolin nor the inhibition by guanyl-5'-ylimidodiphosphate (Gpp(NH)p) of adenylate cyclase activity was not influenced by lithium treatment, suggesting that lithium has no effects on the components of adenylate cyclase system distal to the 5-HT1A receptors. These results indicate that the 5-HT1A-mediated neural transmission has not such an important relevance in the mechanisms of action of lithium or antidepressants.
J Neural Transm Gen Sect 1991
PMID:No alterations in the 5-HT1A-mediated inhibition of forskolin-stimulated adenylate cyclase activity in the hippocampal membranes from rats chronically treated with lithium or antidepressants. 195 90

The functional status of platelet alpha 2-adrenoceptors in patients with major depression has been assessed by simultaneously measuring both a biochemical mechanism of transduction of receptor activation (inhibition of adenylate cyclase activity) and a physiologic response of the receptor (induction of aggregation). The inhibitory effects induced by epinephrine and UK 14304 on adenylate cyclase activity were unchanged, while the aggregation responses induced by the same alpha 2-adrenoceptor agonists were potentiated, which indicated receptor supersensitivity. In depressed (n = 30) and euthymic (n = 11) patients as well as in control subjects (n = 66), there was a clear dissociation between inhibition of adenylate cyclase activity and induction of aggregation, indicating that the two responses represent different phenomena of alpha 2-adrenoceptor activation. alpha 2-Adrenoceptor-mediated platelet aggregation could represent a better marker than inhibition of adenylate cyclase to assess functional changes of the receptor in depression. Both of these functional responses are desensitized after long-term antidepressant treatment.
Arch Gen Psychiatry 1990 Feb
PMID:Alpha 2-adrenoceptor-mediated inhibition of platelet adenylate cyclase and induction of aggregation in major depression. Effect of long-term cyclic antidepressant drug treatment. 196 26

The effect of transient cerebral ischemia and intraventricular injection of kainic acid on adenylate cyclase and protein kinase C as labeled by [3H]forskolin ([3H]FOR) and [3H]phorboldibutyrate ester ([3H]PDBU) in several rat brain microregions was investigated in a quantitative autoradiographic study. Four days after transient four vessel occlusion a 80% loss of [3H]FOR and a 35% loss of [3H]PDBU binding could be measured in the CA1 stratum radiatum of operated Wistar rats as compared to control rats. Four days after intraventricular injection of kainic acid only a marginal loss of [3H]FOR and a 30% increase of [3H]PDBU binding was seen in the CA1 stratum radiatum while in the CA3 stratum lucidum and radiatum respectively a 30% loss of [3H]FOR and no significant change in [3H]PDBU binding was observed. As transient cerebral ischemia and intraventricular kainic acid injection are depleting the hippocampal CA1 region of CA1 pyramidal cells and axons of CA3 pyramidal cells respectively in rat brain, these findings strongly suggest that both adenylate cyclase and protein kinase C are localized in CA1 pyramidal cells of rat hippocampus.
J Neural Transm Gen Sect 1991
PMID:Post- and presynaptic lesions in the CA1 region of hippocampus: effect on [3H]forskolin and [3H]phorboldibutyrate ester binding. 203 10

1. The effects of the diterpene sclareol glycol (SG) of the labdane family on some dopamine (DA) related behavior (locomotor activity in mice, apomorphine-induced stereotypy in mice and rats, and haloperidol-induced catalepsy in rats) were studied. 2. The locomotion frequency of mice was significantly increased by SG (stronger effect by low and medium dose). SG antagonized the hypomotility induced by reserpine pretreatment. SG enhanced the apomorphine decreased motility (induced by small dose of apomorphine). 3. SG provoked increase of apomorphine stereotypy. The long-term SG treatment augmented the sensitivity of rats to apomorphine-induced stereotypy. 4. SG at low dose decreased haloperidol-induced catalepsy: at higher dose it increased the catalepsy. SG treatment alone did not induce catalepsy. 5. These results were discussed in the light of a possible interaction of SG with dopaminergic transmission (DA autoreceptors and postsynaptic DA receptors) at the level of the striatum and the nucleus accumbens. The interaction of SG with adenylate cyclase (stimulation of catalytic subunit) and with GABAergic transmission in realization of its effects on DA related behavior was also discussed.
Gen Pharmacol 1991
PMID:Influences of diterpene sclareol glycol on some dopamine related behavior. 205 29

Human luteinizing hormone (hLH) and the GTP analogue guanosine 5'-O-(3-thio)triphosphate stimulated morphogenesis in the dimorphic fungal pathogen Candida albicans. hLH bound specifically to subcellular fractions from C. albicans and stimulated adenylate cyclase activity in C. albicans microsomes. We provide the first demonstration of guanine-nucleotide-binding proteins (G-proteins) in C. albicans, and propose that the stimulation of C. albicans morphogenesis by hLH is mediated by a receptor-coupled adenylate cyclase system involving G-proteins.
J Gen Microbiol 1990 Nov
PMID:Receptor-mediated elevation of adenylate cyclase by luteinizing hormone in Candida albicans. 207 18

To study the structural arrangement of the chromosomal region containing vir genes of Bordetella pertussis the corresponding 15 kb fragment of Bordetella pertussis chromosomal DNA has been cloned. The sequence homology to an earlier characterized Bordetella pertussis genetical element RSBP1 and flanked by two 400 bp inverted repeats has been shown to be located at an end of a BamHI fragment. The restriction map of Bordetella pertussis 475 coincides with the previously published maps of Bordetella pertussis Tohama and 18323 permitting one to conclude the definite conservatism of the cloned sequence. The preliminary data obtained make possible mapping of the RSBP1 homologous sequence adjacent to adenylate cyclase, agglutinin 2 and pertussis toxin genes. The possible role of RSBP1 elements in the regulation of Bordetella virulence is suggested.
Mol Gen Mikrobiol Virusol 1990 Dec
PMID:[Structural organization of a segment of chromosome, containing the vir gene of Bordetella pertussis]. 208 43

The possibility that arachidonic acid (AA) plays a role in the regulation of steroidogenesis in goldfish was investigated using preovulatory ovarian follicles incubated in vitro. AA was shown to act in a time- and dose-dependent manner to stimulate testosterone production. AA in the range of 10(-5) to 10(-4) M increased testosterone production within 2 hr and had a maximal effect by 9 hr. The magnitude of the testosterone response to AA was similar to that observed when ovarian follicles were incubated with human chorionic gonadotropin (hCG). Ovarian follicles incubated with AA and either hCG or forskolin (adenylate cyclase activator) produced more testosterone than follicles incubated with either of these compounds alone. The actions of AA on testosterone production were completely blocked by cyclooxygenase inhibitors (indomethacin or ibuprofen) and were reduced by 50% by the lipoxygenase inhibitor nordihydroguaiaretic acid. Phospholipase C was far more effective than phospholipase A2 in the stimulation of testosterone production. Taken together, these results suggest that AA formed subsequent to the action of phospholipase C on membrane phospholipids has a role in the regulation of steroidogenesis in preovulatory goldfish ovarian follicles.
Gen Comp Endocrinol 1990 Feb
PMID:Arachidonic acid stimulates steroidogenesis in goldfish preovulatory ovarian follicles. 210 68

The stably BK virus (BKV)-transformed hamster cell line BKT-1B and control BHK-21 cells were treated with dibutyryl cAMP (bu2cAMP), the adenylate cyclase activator forskolin, and the tumour-promoting agent 12-O-tetradecanoylphorbol-13-acetate (TPA). Cultures were stimulated for 30 min (short) and for 24 h (long). Northern blot analysis showed that for bu2cAMP and TPA both short and long stimulation resulted in significant increases in the levels of BKV early transcripts. Short exposure to forskolin resulted in a moderate increase and long exposure in a definite increase. In all cases the increased levels were maintained for at least 24 h after short stimulation was stopped. Experiments including the transcription inhibitor actinomycin D revealed that the enhanced levels of early BKV expression after treatment with the stimuli were due to induced RNA synthesis rather than to stabilization of the RNA. No DNA amplification of the early BKV sequences could be detected in the induced cells. The results are discussed with regard to possible roles for a cAMP-responsive element and a phorbol ester-responsive element, shown by sequencing to be present in the control region of the integrated BKV genome of the BKT-1B cells.
J Gen Virol 1990 Jul
PMID:BK virus early RNA transcripts in stably transformed cells: enhanced levels induced by dibutyryl cyclic AMP, forskolin and 12-O-tetradecanoylphorbol-13-acetate treatment. 216 32


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