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)

Estradiol is shown to induce histidine decarboxylase and histamine to activate adenylate cyclase in the rat uterus. Cyclic AMP like histamine simulates the effect of estradiol, intensifying RNA synthesis and inducing glycolytic enzymes and uterus inhibition. It was found by autoradiography that 3H-estradiol is accepted by the nuclei of some myometrium cells, 3H-histamine by their cytoplasm and 3H-cAMP is selectively bound by endothelium cells of the uterus capillaries. The estradiol messengers (histamine and cAMP) seem to mediate hormonal effect of some uterus heterofunctional cells forming a kind of multicellular functional system.
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PMID:[Multiphasic regulatory system mediating the effect of estradiol in rat uterus]. 22 31

Estradiol receptors are discovered in nuclei, cytoplasm and plasmatic membranes of the target cells. Estradiol activates the transmembrane polyphosphoinositide system: it stimulates the protein kinase C translocation from cytosol to cell membranes, the membrane protein phosphorylation being elevated. Transmembrane adenylate cyclase system is also activated. The cAMP system stimulation by estradiol is mediated by protein kinase C, phosphorylating a protein of adenylate cyclase complex. Estradiol causes protein kinases A translocation into the cell nuclei and enhances the protein kinase NII activity. The role of protein phosphorylation, activated by steroid hormones, in the transcription and protein synthesis regulation, is discussed.
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PMID:[The participation of transmembrane messenger systems in the action of steroid hormones on target cells]. 196 59

The role of growth factor signal transducers in the induction of the progesterone receptor by epidermal growth factor (EGF) and the potential sites of EGF antagonism by an antiestrogen were studied in fetal uterine cells in culture. The effects of EGF and estradiol were not additive, suggesting that EGF and estradiol are acting through common mechanisms where antiestrogens could possibly intervene. Fetal uterine cells in culture were found to contain specific, high affinity binding sites for [125I]EGF. Estradiol treatment of the cells led to a higher number of binding sites, but the site of action of 4-hydroxytamoxifen is not the EGF receptor because this antiestrogen had no effect on EGF binding. Activation of protein kinase C by a phorbol ester (12-O-tetradecanoylphorbol 13-acetate) increased progesterone receptor levels to a similar extent as EGF or estradiol. Increasing the intracellular cAMP concentrations by either adding dibutyryl cyclic AMP or activating adenylate cyclase with forskolin also raised progesterone receptor concentrations. Neither the phorbol ester nor dibutyryl cAMP had any effect on cell proliferation. 4-Hydroxytamoxifen completely abolished the effects of the phorbol ester and cAMP. In conclusion, the levels of an estrogen-induced steroid hormone receptor can be regulated by molecules involved in the signal transduction pathway of peptide factors. Moreover, in fetal uterine cells, a potent antiestrogen appears to act as a multiple antagonist but only on an estrogen-inducible response.
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PMID:Stimulation of progesterone receptors by phorbol ester and cyclic AMP in fetal uterine cells in culture. 215 66

Oviduct adenylate cyclase activity of the quail was measured by radiochemical analysis following different hormonal treatments. A single injection of estradiol benzoate (EB) to immature female quails resulted in a prereplicative surge of adenylate cyclase activity. A second surge of enzyme activity was observed during the proliferative phase induced by EB. Estradiol-17 alpha, estrone, estriol and testosterone were ineffective. Tamoxifen completely inhibits the growth-promoting effect of EB and the second surge of adenylate cyclase activity but does not inhibit the prereplicative increase of enzyme activity. This prereplicative increase of adenylate cyclase activity was also observed, even in the absence of increased plasma estradiol, when estradiol-17 beta (E2) was perfused through the hepatic portal vein. Moreover, E2 had no effect on enzyme activity when added directly to the oviduct homogenate preparation, at concentrations ranging from 10(-9) to 10(-7) M. In response to progesterone injection, oviduct adenylate cyclase activity followed a different pattern, beginning its increase after 3 h and remaining elevated up to 24 h. The activation by estradiol was independent of the presence of guanylylimidodiphosphate. Moreover, the enzyme was more sensitive to forskolin at submaximal concentration in estradiol treated birds than in control. These results demonstrate that transient activation of adenylate cyclase at the early stages of the action of estradiol does not occur through the classic nuclear receptor-gene activation pathway or a membrane receptor mediated process, but involves an indirect pathway, yet to be defined.
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PMID:Modulation of quail oviduct adenylate cyclase activity by estradiol and progesterone. 232 10

Estradiol administration (5 micrograms per day x 4 days) to ovariectomized rats resulted in a 60-70% increase in the maximal lipolytic response of their white adipocytes to isoproterenol, epinephrine, IBMX and forskolin. These altered lipolytic responses were accompanied by parallel changes in the intracellular cyclic AMP levels found in response to 1 mM IBMX alone (+ 106%) or combined with submaximal concentrations of isoproterenol (+205%), epinephrine (+190%) and forskolin (235%). Studies of the adenylate cyclase activity revealed an overall increase in the stimulatory responsiveness of the enzyme (+150 to +200%) after the estradiol-treatment, regardless of the stimulatory agents tested (GTP, GppNHp, fluoride, isoproterenol, ACTH, forskolin). Finally, the finding of a 2-fold enhancement of the Mn2+ (+/- GDP beta S)-stimulated adenylate cyclase activity after the estradiol-treatment strongly suggests that increased activity of the catalytic subunit of this enzyme is the likely mechanism whereby estrogens promote lipolysis in rat fat cells.
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PMID:Increased adenylate cyclase catalytic activity explains how estrogens "in vivo" promote lipolytic activity in rat white fat cells. 245 67

The effect of recombinant human interleukin-1 beta (IL-1 beta) on the follicle stimulating hormone-(FSH) induced secretion of estradiol was investigated using cultured granulosa cells obtained from immature rats with diethylstilbestrol implants. Estradiol secretion was significantly reduced by IL-1 beta in cultures containing FSH and either 10(-7) or 10(-8) M androstenedione as a substrate for estradiol synthesis. However, the inhibition of FSH-induced estradiol secretion by IL-1 beta was more apparent in the presence of 10(-8) M as compared to 10(-7) M androstenedione. IL-1 beta suppressed estradiol secretion during a 72 h culture in a dose-dependent manner with a minimum effective dose of 10 ng/ml. The reduction of FSH-stimulated estradiol secretion by IL-1 beta was greatest after a 48 h culture in the presence of 10(-8) M androstenedione. IL-1 beta did not effect estradiol production when cultures were incubated with various doses of androstenedione in the absence of FSH. Finally, IL-1 beta also suppressed the forskolin-induced secretion of estradiol. These results suggest that IL-1 beta may play some role in the multifactorial regulation of aromatase and estrogen secretion in the early developing follicle, and IL-1 beta may exert an effect on the cAMP-adenylate cyclase messenger system in granulosa cells. Taken together with previous studies, these results provide further evidence for the existence of a putative communications network between the immune and reproductive endocrine systems.
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PMID:Interleukin-1 suppresses follicle-stimulating hormone-induced estradiol secretion from cultured ovarian granulosa cells. 250 16

Primary cultures of anterior pituitary cells from female rats and of mouse embryonic striatal neurons were used to study the effects of 17 beta-estradiol on D1- and D2-dopamine (DA)-sensitive adenylate cyclase. 17 beta-Estradiol pretreatment (10(-9) M, 72 h) suppressed the D2-DA-induced inhibition of adenylate cyclase activity in anterior pituitary cells. The steroid (10(-9) M, 24 h) also blocked the D2-DA-evoked response in striatal neurons whereas it enhanced by twofold the D1-DA-induced stimulation of the enzyme activity in these neurons. All these effects of the steroid were dose dependent and specific, as neither 17 alpha-estradiol, dexamethasone, nor progesterone used at the same concentration (10(-9) M) was effective. Furthermore, the modulation of DA-sensitive adenylate cyclases by the steroid required long-term exposure of living cells to 17 beta-estradiol since neither 17 beta-estradiol pretreatment for 4 h nor its addition to broken cells directly into the adenylate cyclase assay induced any alteration in the DA-sensitive adenylate cyclase activity. These results are in agreement with a genomic effect of the steroid. Using both anterior pituitary cells and striatal neurons in culture, 17 beta-estradiol affected neither the total number of DA (D1 and D2) receptors nor the estimated number of adenylate cyclase catalytic units. Therefore, it is suggested that the steroid modifies the coupling process by a mechanism that still has to be elucidated. These results demonstrate an effect of 17 beta-estradiol on DA target cells in both systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential modulation of D1 and D2 dopamine-sensitive adenylate cyclases by 17 beta-estradiol in cultured striatal neurons and anterior pituitary cells. 252 59

Intrauterine 17 beta-estradiol pellets can induce an up-regulation of guinea pig myometrial beta-adrenergic receptor density and l-isoproterenol-dependent adenylate cyclase activity. Does 17 beta-estradiol influence the ability of beta-adrenergic receptors to form a "high affinity" state with l-isoproterenol, which is a necessary step for adenylate cyclase activation? Nonpregnant, oophorectomized guinea pigs received intrauterine pellets of either placebo, 17 beta-estradiol, progesterone, or 17 beta-estradiol plus progesterone for 1 week. 17 beta-Estradiol resulted in pharmacologic, whereas progesterone resulted in physiologic plasma 17 beta-estradiol and progesterone concentrations, respectively. The affinity of myometrial beta-adrenergic receptors for l-isoproterenol was measured by percentage of inhibition of -[125I]cyanopindolol binding. In all groups, the competition curves in the presence of magnesium chloride could be resolved into two affinity states of the beta-adrenergic receptor, "high" and "low," respectively. The ratio of their dissociation constants was not influenced by hormonal treatment. However, the relative concentration of beta-adrenergic receptors in the high affinity state was significantly higher in the 17 beta-estradiol-treated group than that in the control group. This correlates with the up-regulation in myometrial adenylate cyclase activity and suggests that myometrial beta-adrenergic receptor-adenylate cyclase function may be modulated by 17 beta-estradiol.
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PMID:Treatment of oophorectomized guinea pigs with intrauterine 17 beta-estradiol pellets may modulate myometrial beta-adrenergic receptor binding properties. 257 50

Second (thoracic) mammary glands of endocrine intact mice were removed intact and incubated in Dulbecco's Modified Eagle's Medium supplemented with insulin, aldosterone, and cholera toxin. Insulin and aldosterone resulted in relatively little mammary development. However, insulin, aldosterone, and cholera toxin substantially increased mammary development, as assessed by development scores and DNA after 6 d of culture. Ovariectomy abolished the ability of cholera toxin to augment mammary development in vitro. Estradiol and progesterone injections for 3 d partly restored responsiveness of mammary tissue to cholera toxin, whereas responsiveness was greater after 6 d of injection than in endocrine-intact mice. Additionally, cyclic AMP-dependent protein kinase (kinase A) activity of fourth (inguinal) mammae was increased after as little as 3 d of estradiol and progesterone treatment. Cholera toxin induced phosphorylation of at least one protein was also increased by estradiol and progesterone. Because cholera toxin is a potent activator of adenylate cyclase, these findings suggest that estradiol and progesterone interact with cyclic AMP active agents to promote mammary development. This interaction may be mediated, at least in part, by increased kinase A activity and increased kinase A substrate availability.
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PMID:Estrogen and progesterone augment growth responsiveness of mammary tissue to cholera toxin. 266 40

Estradiol (E2) replacement therapy effectively prevents or delays postmenopausal bone loss, but the mode of E2 action on bone is still unknown. Recently, the presence of E2 receptors was described for bone-derived cells. In this study we examined the estrogen responsiveness of osteoblastic cells using the experimentally immortalized calvarial cell lines RCT-1 and RCT-3 as well as primary cultures of calvarial and trabecular bone cells. E2 treatment reduced PTH-stimulated adenylate cyclase activity by 20-30% in RCT cells; the maximum effect was observed after treatment with 1 nM E2 for 4 h or longer. In trabecular cells E2 decreased PTH-stimulated adenylate cyclase activity by 60-80%. After a lag period of at least 48 h, E2 treatment (0.01-10 nM) increased cell number and [3H]thymidine incorporation in both RCT-3 cells and primary cultures of trabecular cells to 20-60% above control values. Half-maximal effects were observed at about 1 nM E2. Antibodies against insulin-like growth factor-I (IGF-I) inhibited the E2-induced proliferation in a dose-dependent manner without affecting basal growth. Furthermore, E2 treatment increased the steady state levels of IGF-I mRNA 2- to 2.5-fold in calvarial and RCT-3 cells compared to control levels. In addition, E2 (10 nM) increased the level of collagen mRNA more than 2-fold and opposed the suppression of collagen mRNA produced by PTH treatment. The E2 effects were specific to 17 beta-E2, since they were not observed with the biologically less active stereoisomer 17 alpha-E2 and were blocked by the E2 antagonist tamoxifen (1 microM). Thus, for osteoblastic cells in culture, E2 can directly stimulate proliferation as well as collagen and IGF-I mRNA while decreasing PTH responsiveness; these effects could explain the anabolic and anticatabolic effects of E2 on bone.
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PMID:Estradiol effects on proliferation, messenger ribonucleic acid for collagen and insulin-like growth factor-I, and parathyroid hormone-stimulated adenylate cyclase activity in osteoblastic cells from calvariae and long bones. 275 78


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