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)

1. Functional vasoactive intestinal peptide (VIP)/helodermin receptors and beta 2-adrenoceptors coexist in membranes from a cultured cloned BL/VL3 cell line of murine T-cell lymphoma induced by a radiation leukemia virus (see preceding paper in this journal). 2. Short-term (5-30 min) exposures of BL/VL3 cells to VIP or isoproterenol induced both homologous and heterologous desensitization. The potency of VIP and isoproterenol to desensitize was similar to their potency to occupy receptors and activate adenylate cyclase. 3. Long-term (16-h) exposure of BL/VL3 cells to VIP induced homologous down regulation only, whereas isoproterenol induced both homologous and heterologous down regulation. The potency of VIP, peptide histidine isoleucinamide, helodermin, helospectin, and [D-Phe2]VIP on the one hand, and of isoproterenol on the other hand, to decrease homologous responses was comparable to their potency for receptor occupancy and adenylate cyclase activation.
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PMID:Homologous and heterologous regulation of the helodermin/vasoactive-intestinal-peptide response in the murine radiation leukemia-virus-induced lymphoma cell line BL/VL3. 254 7

The vasoactive intestinal peptide (VIP) stimulates adenylate cyclase activity in rat liver and intestinal epithelium with low and high efficacy, respectively. The human growth hormone releasing factor (hGRF) derivative with acetylated N-terminus e.g. Ac-Tyr1hGRF binds to VIP receptors in both tissues with a similar affinity. However, Ac-Tyr1hGRF is a partial VIP agonist with high intrinsic activity in liver (50% that of VIP) whereas it behaves as a VIP antagonist in intestine. These results further argue for a possible heterogeneity of VIP receptor-coupled adenylate cyclase among tissues on a pharmacological basis.
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PMID:Ac-Tyr1hGRF discriminates between VIP receptors from rat liver and intestinal epithelium. 254 22

We have recently shown the presence of adenosine receptors coupled to adenylate cyclase in anterior pituitary and in the present studies we have investigated the effects of adenosine on ACTH release. The 'R'-site specific analogs of adenosine such as N-Ethylcarboxamide adenosine (NECA), L-N6-phenylisopropyl adenosine (PIA), 2-chloro-adenosine (2-Cl-Ado) all stimulated ACTH release in a dose-dependent manner. NECA was the most potent analog and stimulated ACTH release by about 170% with an apparent Ka of 0.1 microM, whereas PIA and 2-Cl-Ado were less potent and stimulated the release by about 110% and 125% with an apparent Ka of 0.2 and 0.4 microM respectively. The stimulation of ACTH release by NECA was inhibited by 3-isobutyl-1-methylxanthine (IBMX). On the other hand, adenosine deaminase (ADA) treatment of the cells also stimulated ACTH release as well as adenylate cyclase activity by about 2-fold, suggesting that endogenous adenosine plays an inhibitory role in the release of ACTH. Other agents, such as corticotropin-releasing factor (CRF), vasoactive intestinal peptide (VIP) and forskolin (FSK) also stimulated ACTH release from these cells. In addition, the stimulation by an optimal concentration of NECA was almost additive with maximal stimulation caused by VIP and FSK. These data suggest that adenosine modulates ACTH release from anterior pituitary through its interaction with adenosine receptors coupled to adenylate cyclase.
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PMID:Adenosine regulates the release of adrenocorticotropic hormone (ACTH) from cultured anterior pituitary cells. 255 Jul 86

Fetuses were investigated to establish whether vasoactive intestinal peptide (VIP) and its receptors are involved in the basic biochemical defect causing cystic fibrosis (CF). The intestine was used as a target for the disease and the liver as control. The immunoreactive and biologically active VIP contents of the colon and lower part of the small intestine were 1.5-2.5 times higher in CF fetuses than in controls. In control and CF intestinal mucosa, there was no change in the Scatchard parameters of the 125I-labeled VIP binding sites (Kd = 4.7-6.1 X 10(-11) M; Bmax = 268-280 fmol/mg protein for the high-affinity sites), in the two molecular components constituting the cross-linked 125I-VIP binding (Mr = 66,000 and 30,000), or in the pharmacological properties and functional characteristics of the VIP receptors activating the G proteins-adenylate cyclase system (Ka = 0.7 X 10(-9) M VIP). Similar results were obtained in liver. These findings suggest that neither VIP nor its receptors are involved in CF intestine. The possible involvement of other effectors related to the VIP pathway in CF intestine, including the release of VIP and adenosine 3',5'-cyclic monophosphate signal-transduction cascade, are presented.
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PMID:Vasoactive intestinal peptide and its receptors in fetuses with cystic fibrosis. 255 25

Previous studies have demonstrated a specific vascular receptor for the neurotransmitter peptide, vasoactive intestinal peptide (VIP), and have suggested that the receptor is positively coupled to vascular adenylate cyclase. The present study addressed the questions whether the vascular VIP receptor is subject to regulation by guanine nucleotides and whether a disulfide reducing agent, dithiothreitol, would perturb the binding function of the vascular VIP receptor. Guanosine triphosphate (GTP) and its non-hydrolyzable analogs, guanylyl imidodiphosphate (Gpp(NH)p) and guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma-S), increased the rate of dissociation of radiolabeled VIP from arterial receptors in a concentration-dependent manner. GTP-gamma-S increased the equilibrium dissociation constant (KD) of the high affinity vascular VIP binding site, a result consistent with decreased high affinity binding of VIP induced by GTP-gamma-S. These results are consistent with a regulatory role for guanine nucleotides in the function of the vascular VIP receptor. The disulfide reducing agent, dithiothreitol, caused a decrease in specific binding of radiolabeled VIP. Upon Scatchard analysis the effect of dithiothreitol was characterized by an increase in the KD and a decrease in the maximum number of binding sites (Bmax) of the high affinity binding site. These results suggest that disulfide bonds are important for ligand binding to vascular VIP receptors. The sulfhydryl alkylating agents, N-ethylmaleimide and iodoacetamide, had minimal effects on radioligand binding.
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PMID:Effects of GTP analogs and dithiothreitol on the binding properties of the vascular vasoactive intestinal peptide receptor. 255 41

1. Catecholamines, adenosine, gonadotrophins, vasoactive intestinal peptide (VIP) and E-series prostaglandins all elicit K+ currents in follicle-enclosed Xenopus oocytes. Evidence suggests that cyclic nucleotides act as intracellular messengers in the activation of this K+ conductance. Muscarinic agonists and some divalent cations (e.g. Co2+, Mn2+, Ni2+ and Cd2+) elicit slow oscillatory Cl- currents, which are activated through hydrolysis of inositol phospholipids and mobilization of intracellular calcium by inositol phosphates. 2. We investigated whether these membrane current responses were generated in the oocyte itself or in enveloping follicular cells which are coupled to the oocyte by gap junctions. Oocytes were defolliculated, either enzymatically using collagenase, or by manual dissection combined with rolling over poly-L-lysine-coated slides. Removal of follicular cells was checked using scanning electron microscopy. Membrane current responses of defolliculated oocytes were compared with responses seen in follicle-enclosed oocytes taken from the same ovary. 3. The K+ responses evoked by all the various hormones/neurotransmitters were either drastically reduced (greater than 90%) or abolished by defolliculation. K+ currents generated by the adenylate cyclase activator forskolin and by intraoocyte injection of adenosine 3',5'-cyclic monophosphate (cyclic AMP), or guanosine 3',5'-cyclic monophosphate were similarly reduced in defolliculated oocytes. In contrast, oscillatory Cl- currents to acetylcholine and divalent cations were selectively preserved through defolliculation. 4. Injection of cyclic AMP (1-20 pmol) into defolliculated oocytes had little or no effect on oscillatory Cl- currents elicited by ACh. However, the calcium-dependent transient Cl- current, activated by depolarization of the oocyte membrane, was consistently potentiated (100-900%) by injections of cyclic AMP (1-10 pmol). 5. These experiments suggest that cyclic nucleotide-activated K+ currents arise essentially in follicular cells and are monitored within the oocyte through electrical coupling by gap junctions. Oscillatory Cl- responses evoked by ACh and divalent cations are produced largely or wholly in the oocyte itself.
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PMID:Effects of defolliculation on membrane current responses of Xenopus oocytes. 255 77

Different peptide hormones influence hormone secretion in pituitary cells by diverse second messenger systems. Recent data indicate that luteinizing-hormone-releasing hormone (LHRH) stimulates and somatostatin inhibits voltage-dependent Ca2+ channels of GH3 cells via pertussis-toxin-sensitive mechanisms [Rosenthal et al. (1988) EMBO J. 7, 1627-1633]. In other pituitary cell lines, somatostatin has been shown to cause a pertussis-toxin-sensitive decrease in adenylate cyclase activity, and LHRH and thyrotropin-releasing hormone (TRH) stimulate phosphoinositol lipid hydrolysis in a pertussis-toxin-independent manner. Whether stimulation of Ca2+ influx by TRH is affected by pertussis toxin is not known. In order to elucidate which of the hormone receptors interact with pertussis-toxin-sensitive and -insensitive G-proteins, we measured the effects of LHRH, somatostatin and TRH on high-affinity GTPases in membranes of GH3 cells. In control membranes, both LHRH and TRH stimulated the high-affinity GTPase by 20%, somatostatin by 25%. Maximal hormone effects were observed at a concentration of about 1 microM. Pretreatment of cells with pertussis toxin abolished pertussis-toxin-catalyzed [32P]ADP-ribosylation of 39-40-kDa proteins in subsequently prepared membranes and reduced basal GTPase activity. The toxin also reduced by more than half the increases in GTPase activity induced by LHRH and TRH; stimulation of GTPase by somatostatin was completely suppressed. Stimulation of adenylate cyclase by vasoactive intestinal peptide (VIP) was not impaired by pretreatment of cells with pertussis toxin. Somatostatin but not LHRH and TRH decreased forskolin-stimulated adenylate cyclase activity. The results suggest that the activated receptors for LHRH and TRH act via pertussis-toxin-sensitive and -insensitive G-proteins, whereas effects of somatostatin are exclusively mediated by pertussis-toxin-sensitive G-proteins.
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PMID:Secretion-stimulating and secretion-inhibiting hormones stimulate high-affinity pertussis-toxin-sensitive GTPases in membranes of a pituitary cell line. 256 42

The effects of two hormones, vasopressin and somatostatin (SOM), on ion secretion in rat colon descendens were compared. Three modes for induction of epithelial secretion were used: neuronally mediated secretion due to electric field stimulation (EFS), Ca2+-dependent secretion elicited by carbachol, and cAMP-dependent secretion evoked either by a receptor-mediated mechanism elicited by vasoactive intestinal peptide (VIP) or by a direct activation of the adenylate cyclase by means of forskolin. Somatostatin inhibited ion secretion evoked by EFS (55-65%), carbachol (80%) and VIP (95%) in a dose-dependent manner. Maximal inhibition by SOM was observed at 10(-7) M. Somatostatin had, however, no effect on the secretory response to forskolin. The inhibition of the VIP effect could be attenuated by pretreatment with pertussis toxin. In contrast, vasopressin in concentrations as low as 0.025-0.25 U/liter decreased the secretory effects of EFS (55-75%) and carbachol (85%), but had no effect on cAMP-dependent secretion elicited either by VIP or forskolin. The results suggest that the antisecretory effect of vasopressin is mediated only by a block in the Ca2+ pathway, whereas SOM inhibits Ca2+-dependent secretion as well as receptor-mediated cAMP-dependent secretion. The interaction with the cAMP pathway is located at the step between stimulation of the receptor and activation of the adenylate cyclase and probably involves an Ni-protein.
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PMID:Antisecretory effects of somatostatin and vasopressin in the rat colon descendens in vitro. 256 91

The effect of vasoactive intestinal peptide (VIP) and related peptides [glucagon, secretin, PHI 1-27 (peptide with N-terminal histidine and C-terminal isoleucine)] on renal adenylate cyclase (AC) has been determined in several species. The largest stimulation (4.1 +/- 0.5-fold basal) of AC by 1 mumol.l-1 VIP was observed in feline cortical plasma membranes. In rabbit and guinea-pig, VIP increased AC activity 1.5 +/- 0.3- and 1.8 +/- 0.3-fold respectively but glucagon had no such action. Conversely in the rat glucagon stimulated AC some 3-fold over basal activity whereas VIP had little effect. In dog, cat and mouse both peptides were effective in increasing AC activity. For cat, half-maximal stimulation of cortical plasma membrane AC by VIP was seen at 27.0 +/- 9.0 nmol.l-1 (SE N = 9 animals). VIP also increased AC activity in both outer (red) and inner (white) medulla. In feline cortical membranes VIP and PTH (parathyroid hormone) when added in combination were fully additive. However for VIP and glucagon in combination there was no cumulative increase in AC activity, indeed the resultant activity was less than that attained by VIP alone. The VIP analogue (4Cl-D-Phe6Leu17)VIP at 10 mumol.l-1 produced a right shift in the VIP-dose response curve and increased the EC50 from 17.2 +/- 5.8 nmol.l-1 to 132.0 +/- 22.2 nmol..-1 VIP (SE N = 4). There was no reduction in the maximum response elicited by VIP consistent with a competitive type of antagonism by this analogue. PHI-stimulated AC was also reduced by (4Cl-D-Phe6Leu17)VIP resulting in a similar right shift in the dose response curve.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasoactive intestinal peptide stimulation of renal adenylate cyclase and antagonism by (4Cl-D-Phe6Leu17)VIP. 275 76

Peculiarities in hormonal regulation of adenylate cyclase (AC) were studied in large bowel tumors to establish criteria of their hormonal dependence. The investigation showed a diminished basal activity of AC matched by decreased response to sodium fluoride, glucagon, and vasoactive intestinal peptide (VIP) in tumors as compared with normal intestinal mucosa. Some cases revealed an increased response of AC to a nonspecific ("inappropriate") stimulator--calcitonin. This was rather typical of colonic tumors while a diminished response to specific ("appropriate") stimulation by VIP and glucagon was more frequent in rectal cancer. The results showed a relationship between hormonal regulation of AC activity and lipid composition of tumor tissue, thus suggesting the possibility of influencing the hormone dependence of intestinal tumors by drugs used to eliminate disturbance of fat-carbohydrate metabolism.
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PMID:Peculiarities of hormonal regulation of adenylate cyclase and lipid composition in colonic and rectal tumors. 277 Sep 32


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