Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An adenylate cyclase activity (AC) was found in guinea pig brown adipose tissue (BAT), since the tissue's apparition. This enzymatic activity increased during the development and showed high values at the end of gestation. An increase of AC units per cell was observed, in addition to the cell multiplication. A norepinephrine stimulation of AC activity was observed at the end of gestation : this regulating action disappeared in the first days of extrauterine life. Neither glucagon nor ACTH had any regulating role upon AC activity during fetal and newborn life. The basal lipolytic activity which was observed in BAT of fetuses (61rst day) and neonate dramatically around the 15th day. A potent lipolysis activation by norepinephrine was observed, but only after birth. The correlation observed between these enzymatic activities in presence of norepinephrine seems to indicate that the AC/lipase system was involved in the neonatal thermogenesis of guinea pigs.
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PMID:[Adenylate cyclase/Lipase. Hormone receptor induction]. 17 89

Purified adipocytes plasma membranes have been prepared from human adipose tissue. The presence of an adenylate cyclase sensitive to epinephrine and fluoride has been demonstrated. Activation of the adenylate cyclase was usually 2 to 4 fold in the presence of epinephrine 5.10-5M and 8 to 10 fold in the presence of fluoride 10 mM. The adenylate cyclase from human adipose tissue was insensitive to glucagon and ACTH; these results are in support of previous studies of lipolysis in isolated fact cells or tissue fragments from human adipose tissue.
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PMID:Activity of human adenylate cyclase from human fat cell membranes. 17 15

ACTH stimulated steroidogenesis and cAMP (adenosine 3',5'-monophosphate) accumulation in an adrenocortical mouse tumor cell line (clone Y1) with Kd values which differed by more than one order of magnitude (5.2 X 10(-11) M and 7 X 10(-10) M, respectively). All of the cAMP formed in response to added ACTH appeared extracellularly in 5- or 30-min incubations. ACTH, at 5 and 10 muU/ml, stimulated steroidogenesis to 25% and 40% of maximum activity; and increased the extracellular accumulation of cAMP 1.4-fold and 2.3-fold, respectively. The effects of ACTH appeared to be via an action on intracellular ATP, specific for cAMP and dependent on an ACTH-sensitive adenylate cyclase system. These observations indicate that ACTH increases cAMP accumulation in Y1 cells at virtually all steroidogenic concentrations and suggest that cAMP is an essential component of ACTH-stimulated steroidogenesis.
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PMID:Steroidogenesis and extracellular cAMP accumulation in adrenal tumor cell cultures. 17 21

Adenyl cyclase activity of rat pancreatic islet membrane was increased by secretin, pancreozymin, and isoproterenol, while ACTH, glucagon, growth hormone, and insulin had no effect. Both secretin and isoproterenol activations were enhanced by prostaglandin E1 (PGE1) and GTP. Isoproterenol activation was additive with PGE1, as was that of secretin with PGE1, but only in the presence of GTP. Secretin activation in the presence of PGE1 and GTP was equivalent to NaF stimulation. Kinetic analysis indicated that secretin and GTP increased the maximum velocity of the adenyl cyclase and tended to decrease the apparent affinity of the enzyme for ATP. Glucagon activation of islet membrane adenyl cyclase was dependent upon prior treatment of the membrane preparation with EGTA and the use of inhibitors of proteolytic enzymes during the collagenase digestion phase of islet preparation. These results suggest that hormonal regulation of insulin secretion may be affected by PGE1 and guanine nucleotide modulation of the adenyl cyclase activation process.
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PMID:Hormonal regulation of pancreatic islet adenyl cyclase. 17 51

The ability of three analogs of ACTH1-24 ([Gln5, Phe9] ACTH1-24, [Gln5, Ala9[Acth1-24, and [Gln5, Lys8, Phe9[ ACTH1-24) embodying tryptophan substitutions to activate the adenylate cyclase system of a bovine adrenal plasma membrane preparation was compared to the effect of the analogs on adenosine 3':5'-monophosphate (cyclic AMP) accumulation and steroidogenesis in viable bovine adrenocortical cells. The results were not comparable. Whereas the analogs antagonized the ACTH1-24-activated membrane cyclase they stimulated cyclic AMP accumulation as well as steroid production of the cells. None of the analogs inhibited steroidogenesis of ACTH1-24-stimulated cells, but two of them, at very high dose levels, inhibited cyclic AMP production. The ability of the analogs to stimulate steroidogenesis of the adrenal cells half-maximally decreased in the order tryptophan greater than phenylalanine greater than alanine, indicating that the aromaticity of the indole ring of tryptophan is necessary for maximal interaction between hormone and receptor. Both the absolute and relative steroidogenic potencies were the same for several analogs when assayed with rat adrenal cells. Although only a small fraction of the cell's potential to produce cyclic AMP was necessary to induce maximum steroid production, the relative activities of a series of analogs were the same for steroidogenesis as for cyclic AMP accumulation. Furthermore, the concentration of cyclic AMP necessary for full steroidogenesis was practically identical for a series of peptides that differed widely in potency. These findings support the postulate that cyclic AMP accumulation and steroidogenesis in adrenocortical cells are coupled processes. The differential behavior of bovine adrenal plasma membranes and bovine adrenocortical cells toward ACTH analogs indicates that structure-function studies using cyclase assays may not reflect events that take place in the intact adrenal or in cell preparations derived therefrom.
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PMID:Differential response to adrenocorticotropic hormone analogs of bovine adrenal plasma membranes and cells. 18

Isoproterenol, corticotropin (ACTH), and triodothyronine immobilized on glass and Sepharose beads by diazotization procedures have been shown to interact with cultured tumor cells of "target tissue" origin. Cells used were rat glioma cells (C6), rat adrenal tumor cells (Y-1), and rat pituitary tumor cells (GH3). The rat glioma cells bound principally to immobilized isoproterenol, whereas the rat adrenal tumor cells bound to immobilized corticotropin, and rat pituitary tumor cells bound to immobilized triiodothyronine. Binding was inhibited by preincubation of the cells in soluble drug or hormone. With C6 cells there was a positive correlation between adenylate cyclase [ATP pyrophosphate-lyase (cyclizing, EC 4.6.1.1] stimulation and the degree of binding to the immobilized isoproterenol. Norepinephrine, bound through the ethanolamine side chain via an amide linkage, did not bind cells, demonstrating specific structural requirements for drug-cell interactions. HeLa cells were shown to bind tightly to diphtheria toxin coupled to Sepharose beads via an amide bond. This binding was inhibited by prior incubation of the Sepharose toxin with purified antitoxin. Toxin bound to Sepharose via an azo bond did not bind cells. These data suggest that the cell affinities are due to cell surface receptors interacting with the immobilized drugs and hormones, and that the observed affinities possibly reflect the relative receptor complement of these cells.
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PMID:Affinity isolation of cultured tumor cells by means of drugs and hormones covalently bound to glass and Sepharose beads. 18 May 34

Experiments in vitro on tissue from a feminizing adrenocortical carcinoma removed from a postmenopausal patient are described. Portions of the adrenal tumor were cultured. The effects of ACTH, prolactin, and other protein hormones on the synthesis and secretion of steroid hormones by the cultured tissue were studied. Steroids were extracted from the culture medium with ethyl acetate. Steroid production was determined by high resolution-mass fragmentography and by radioimmunoassay. Results suggest that in vitro neither growth hormone (GH) nor luteinizing hormone (LH), at the concentrations used, effectively stimulated the synthesis and secretion of estradiol-17beta by the adrenal tumor tissue. However, ACTH and prolactin with insulin, appearing to influence the action of both these hormones, stimulated the output of estradiol-17beta. Steroid was being synthesized during the 3-day culture period. The tumor tissue actively synthesized and secreted into the medium estrone as well as estradiol-17beta under the influence of ACTH and prolactin with insulin. Data also suggest that LH and GH were capable of influencing the synthesis and secretion of androstenedione by the tissue explants. No DNA sulphate was present in the media from the tumor tissue cultures before or after incubation with either ACTH or prolactin. Results from studies with normal adrenal tissue in culture indicated that DNA sulphate, DHA, and androstenedione were present in the culture medium after 3 days' incubation. In this report the concentration of endogenous estrone relative to estradiol-17beta and estradiol was found to be high. The effect of protein hormones, other than ACTH, on adenylate cyclase activity of this tumor tissue indicated a lack of specificity of the membrane receptor sites. High resolution-mass fragmentography had greater specificity than radioimmunoassay.
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PMID:In vitro synthesis of steroids by a feminising adrenocortical carcinoma: effect of prolactin and other protein hormones. 18 Jul 40

The chelator EGTA inhibits the activation of bovine adrenal cortex adenylate cyclase by ACTH. Hormonal response is restored by addition of Ca2+, Mn2+ and other cations which are able to significantly reduce the concentration of uncomplexed EGTA in the adenylate cyclase assy medium. Time course studies reveal that the enzyme in the activated state (induced by adenylate cyclase reagents and hormone or by pretreatment with hormone) is resistant to EGTA inhibition.
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PMID:Adrenal cortex adenylate cyclase. Is Ca2+ involved in ACTH stimulation? 18 84

The effects of cholera on adrenal weight in hypophysectomized rats were investigated, in an attempt to demonstrate an ACTH-like, adrenal trophic effect of the toxin. The results suggested that the toxin probably exerts is ACTH-like action on the adrenal via adenylate cyclase. Cholera toxin was also shown to have a thermolytic action, similar to that of ACTH, probably due to stimulation of adrenal glucocorticoid secretion.
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PMID:The effects of cholera toxin on the adrenal weight in hypophysectomized rats. 18 72

1. We have shown differences in hormonal regulation of adenylate cyclase activity in fat cell ghosts prepared from rat, rabbit, fox and badger adipose tissue, under the influence of catecholamines, ACTH and insulin. a) In the rat, catecholamines induced a large stimulation (+315%) of adenylate cyclase. b) In the rabbit, ACTH was the most effective hormone. c) In the fox and the badger, only catecholamines could stimulate adenylate cyclase. d) In both rat and rabbit, insulin did not reduce spontaneous enzymatic activity. Moreover, the activation of adenylate cyclase by ACTH in the rabbit was not altered by insulin, while in the rat, this hormone slightly decreased epinephrine stimulation. 2. Hormonal regulation of adenylate cyclase correlated with the lipolytic response.
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PMID:[Hormonal control of the adenyl cyclase activity of adipose cell membranes prepared from badger, rabbit, fox and rat adipose tissues]. 18 72


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