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)

Neuroblastoma-glioma NG108-15 cells that were cultured for 48 h with the opiate antagonist, naloxone, respond to the guanosine 5'-triphosphate (GTP) analogue guanosine 5'-[beta, gamma-imido]-triphosphate (GMP-PNP) in the binding assay as the control, non-treated, cells. This was observed when the guanyl nucleotide was tested in the presence or absence of sodium chloride and also after subcellular fractionation of the membranes on a sucrose gradient which separated between two receptor-containing fractions. The findings suggest that the increase in delta type enkephalin receptors in naloxone-treated NG108-15 cells does not reflect an alteration in the interaction between the receptor and the adenylate cyclase-GTP-binding protein system.
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PMID:Up-regulation of opiate receptors by opiate antagonists in neuroblastoma-glioma cell culture: the possibility of interaction with guanosine triphosphate-binding proteins. 609 9

A procedure for isolating a suspension of tubules derived from the rabbit medullary thick ascending limb is described. The purity of the preparation was assessed by microscopy and enzyme assays and the viability of the preparation was assessed by measuring oxygen consumption. Microscopy revealed that the suspension contains 95% thick ascending limbs and that the isolation procedure preserves the structure of the epithelium except for the loss of the basement membrane. The preparation had a high activity of calcitonin-sensitive adenylate cyclase, a marker enzyme for the medullary thick ascending limb. Control oxygen consumption was considerably higher than that reported for proximal tubules in the literature, and nystatin or carbonyl cyanide p-trifluoromethoxyphenylhydrazone addition produced a more than 100% increase in oxygen consumption. Furosemide inhibited the oxygen consumption by 43% and ouabain inhibited it by 42%. Furosemide inhibited sodium chloride entry without directly affecting the Na-K-ATPase or cellular metabolism. Chloride removal depressed oxygen consumption to the same extent as furosemide, but some of this action was through direct inhibition of cellular metabolism.
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PMID:Suspension of medullary thick ascending limb tubules from the rabbit kidney. 609 84

Although acute alterations in Ca2+ fluxes may mediate the skeletal responses to certain humoral agents, the processes subserving those fluxes are not well understood. We have sought evidence for Ca2+-dependent ATPase activity in isolated osteoblast-like cells maintained in primary culture. Two Ca2+-dependent ATPase components were found in a plasma membrane fraction: a high affinity component (half-saturation constant for Ca2+ of 280 nM, Vmax of 13.5 nmol/mg per min) and a low affinity component, which was in reality a divalent cation ATPase, since Mg2+ could replace Ca2+ without loss of activity. The high affinity component exhibited a pH optimum of 7.2 and required Mg2+ for full activity. It was unaffected by potassium or sodium chloride, ouabain or sodium azide, but was inhibited by lanthanum and by the calmodulin antagonist trifluoperazine. This component was prevalent in a subcellular fraction which was also enriched in 5'-nucleotidase and adenylate cyclase activities, suggesting the plasma membrane as its principal location. Osteosarcoma cells, known to resemble osteoblasts in their biological characteristics and responses to bone-seeking hormones, contained similar ATPase activities. Inclusion of purified calmodulin in the assay system caused small non-reproducible increases in the Ca2+-dependent ATPase activity of EGTA-washed membranes. Marked, consistent calmodulin stimulation was demonstrated in membranes exposed previously to trifluoperazine and then washed in trifluoperazine-free buffer. These results indicate the presence of a high affinity, calmodulin-sensitive Ca2+-dependent ATPase in osteoblast-like bone cells. As one determinant of Ca2+ fluxes in bone cells, this enzyme may participate in the hormonal regulation of bone cell function.
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PMID:A high affinity, calmodulin-responsive (Ca2+ + Mg2+)-ATPase in isolated bone cells. 613 20

In intact LLC-PK1 cells, occupancy of vasopressin receptors (Roy, C., and Ausiello, D. A. (1981) J. Biol. Chem. 256, 3415-3522) correlated with cell cAMP production. This relationship was observed as a function of hormone dose, incubation time, and changes in receptor affinity. However, the rate of cAMP production diminished with time in intact cells exposed to high hormone concentrations, even in the presence of a phosphodiesterase inhibitor. A rapid desensitization of adenylate cyclase activity was observed in minutes upon treatment of intact cells with high hormonal concentrations. Desensitization was dose- and time-dependent. Hypertonic sodium chloride, which increased hormonal binding and cell cAMP production, prevented desensitization. The acute decrease in hormone-stimulated adenylate cyclase activity correlated with increased occupancy of low affinity binding sites. EDTA-suspended cells, which have a homogeneous population of binding sites, did not demonstrate desensitization. A proposal is made as to the consequences of this phenomenon at physiological concentrations of vasopressin.
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PMID:Relationship of (8-lysine) vasopressin receptor transition to receptor functional properties in a pig kidney cell line (LLC-PK1). 616 46

A homogeneous population of single cells from the thick ascending limb of Henle's loop (TALH) has been isolated from the rabbit kidney medulla. A total medullary cell suspension was prepared by a series of collagenase, hyaluronidase, and trypsin digestions and separated on a Ficoll gradient (2.6-30.7% wt/wt). Morphologically, the cells isolated from the TALH were homogeneous and showed polarity within their plasma membrane structure, with a few blunt microvilli on their apical surface and deep infoldings of the basal-lateral membrane. Biochemically, the TALH cells were highly enriched in calcitonin-sensitive adenylate cyclase and Na, K-ATPase. Alkaline phosphatase and arginine vasopressin-sensitive adenylate cyclase, highly concentrated in proximal tubule and collecting duct, were present only in low concentrations in the TALH cells. Additionally, furosemide, a diuretic inhibiting sodium chloride transport in the TALH in vivo, inhibited oxygen consumption of the TALH cells in a dose-dependent manner. The TALH cells were viable, as judged by morphological appearance, trypan blue exclusion, the response of oxygen consumption to 2,4-dinitrophenol, succinate and ouabain, and the cellular Na, K and ATP levels.
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PMID:Separation of renal medullary cells: isolation of cells from the thick ascending limb of Henle's loop. 625 27

Osmotically balanced solutions of sodium chloride and glucose (5-150 mmol/l) were instilled into rats prepared with two tied intestinal loops (jej-col or il-col). Luminal accumulation or disappearance of Na and glucose after 15 min. was determined, and the parameters of the linear regression lines of net Na flux (y) with initial Na concentration (x) calculated. Control cation and glucose transport were changed by dioctylsulphosuccinate and dodecylsulphate in the way described by Sund & Matheson (1978). Theophylline (10-25 mmol/l) on the other hand did not alter glucose disappearance, and had a distinctly dissimilar effect on net Na transport compared to the surfactants. This could be described as a parallel displacement of the control regression lines to the right, without improvement in correlation. This effect of theophylline was greatest in the ileum, where mean luminal Na concentration corresponding to zero net transport was raised from about 70 mmol/l under control condition to values above 200 mmol/l. The results are consistent with the view that theophylline mainly affects transcellular and the surfactants mainly paracellular sodium transport, and do not support the theory that the effect of dioctylsulphosuccinate on intestinal transport is related to an activation of the mucosal adenylate cyclase/cAMP system, at least not in short term experiments.
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PMID:Net sodium and glucose transport in the jejunum, ileum and colon of anaesthetized rats in response to intraluminal theophylline and anionic surfactants. 627 35

The effects of increasing mucosal or serosal concentrations (1-4 mM) of taurochenodeoxycholate (TCDC) on sodium chloride transport across the isolated, short-circuited rabbit colon were examined. Mucosal TCDC produced dose-related increases in tissue conductance (Gt) and the unidirectional fluxes of Na+ and Cl- and dose-related decreases in net NaCl absorption. At 4 mM mucosal TCDC, Gt was increased fivefold, net sodium flux (JNanet) was reduced 50%, and JClnet was abolished. Serosal TCDC also produced dose-dependent changes in permeability that were quantitatively different. Four millimolar serosal TCDC produced a 2.7-fold increase in Gt, abolished JNanet, and stimulated electrogenic Cl- secretion. TCDC-induced Cl- secretion was stimulated by 10(-5) M serosal TCDC, inhibited by serosal furosemide or ouabain, did not alter theophylline-induced secretion (and vice versa), and occurred in the absence of serosal Ca2+. It is suggested that 1) TCDC inhibition of sodium absorption is indirect (i.e., not simply due to a reduction in the activity of the Na "pump," since Cl- secretion persists during conditions that abolish JNanet) and 2) TCDC induces Cl- secretion by enhancing the activity of basolateral membrane adenylate cyclase.
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PMID:Dihydroxy bile salt-induced alterations in NaCl transport across the rabbit colon. 666 Mar 1

The diterpene forskolin has been shown by Seamon et al (Proc. Natl. Acad. Sci., USA, 78: 3363-3367, 1981) to elicit a large increase in adenylate cyclase activity and to permit further activation by GTP, GDP, sodium fluoride and hormones. The present communication documents forskolin activation of adenylate cyclase activity in hamster adipocyte membrane preparations and shows that the forskolin activated enzyme remains susceptible to inhibition by prostaglandin E1 and clonidine. Moreover, the presence of forskolin, while causing stimulation of adenylate cyclase activity does not appear to prevent the interactions of sodium chloride and GTP with the enzyme. Thus, sodium chloride increased both basal and forskolin stimulated adenylate cyclase activity while GTP decreased activities of the sodium chloride and forskolin activated enzymes. Attenuation of adenylate cyclase activity with clonidine and prostaglandin E1 was detected in the presence of forskolin and GTP and sodium chloride were required. The concentration of GTP required to decrease adenylate cyclase activity and to allow attenuation of the enzyme activity by prostaglandin E1 was not altered by the addition of forskolin.
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PMID:Inhibition of forskolin activated adenylate cyclase in hamster adipocyte membranes with prostaglandin E1 and clonidine. 689 78

The modulation of dopamine DA1 receptors of cultured rat renal arterial smooth muscle cells by glucocorticoid and sodium chloride was studied. At a concentration of 10 nM, the synthetic glucocorticoid dexamethasone increased maximum receptor binding but had no effect on the dissociation constant. However, the maximum binding of [3H]Sch-23390 in cells treated with 100 mM sodium chloride did not change. However, the dissociation constant for DA1 receptor was increased by adding sodium chloride. The glucocorticoid effect on DA1 of arterial smooth muscle cells became apparent after hours of incubation in the presence of the steroid and was significantly inhibited by cycloheximide (10 micrograms/ml) or by the glucocorticoid receptor antagonist RU-38486, indicating that the effect required protein synthesis through glucocorticoid receptors. Treatment of cells with 1 microM dexamethasone for 24 h increased basal and DA1-stimulated adenylate cyclase activity. Basal adenylate cyclase was decreased by sodium chloride in a dose-dependent manner. These results suggest differential control of DA1 receptors on vascular smooth muscle cells by glucocorticoid or sodium chloride.
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PMID:Dopamine DA1 receptors on vascular smooth muscle cells are regulated by glucocorticoid and sodium chloride. 809 5

The modulation of dopamine DA1 receptors of cultured rat renal arterial smooth muscle cells by phorbol ester, glucocorticoid and sodium chloride was studied. The extent of [3H]Sch-23390 binding to phorbol ester-treated cell was increased without any change in the dissociation constant (Kd). At a concentration of 10 nmol/l, the synthetic glucocorticoid dexamethasone increased maximum receptor binding (Bmax) but had no effect on the Kd. 100 mmol/l sodium chloride did not change Bmax, but increased the Kd for DA1 receptor. The production of cAMP in response to DA1 receptor stimulation was enhanced without any change of the adenylate cyclase activity. The glucocorticoid effect on DA1 of arterial smooth muscle cells became apparent after hours of incubation in the presence of the steroid and was significantly inhibited by cycloheximide (10 micrograms/ml) and by the glucocorticoid receptor antagonist RU-38486, indicating that the effect required protein synthesis through glucocorticoid receptors. Treatment of cells with 1 mumol/l dexamethasone for 24 h increased basal and DA1-stimulated adenylate cyclase activity. Basal adenylate cyclase was decreased by sodium chloride in a dose-dependent manner. These results suggest differential control of DA1 receptors on vascular smooth muscle cells by protein kinase C, glucocorticoid or sodium chloride.
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PMID:Vascular dopamine-I receptors. 852 70


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