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)

A somatomammotropic cell line (P0) derived from adult rat pituitaries has been maintained in culture for 2 yr. Secretion of GH and PRL by this cell line has been studied in response to hypophysiotropic peptides known to affect the release of both hormones as well as agents that affect second messenger systems in an attempt to characterize the stimulus-secretion mechanisms used by these cells. GH and PRL release during short term (4 h) incubations of P0 cells and primary cultures of dispersed rat pituitary cells was initially measured in response to GRF, TRH, vasoactive intestinal peptide (VIP), and SRIF. In P0 cells, the minimal effective dose of each of the hypophysiotropic peptides was comparable with respect to GH and PRL secretion. The effects of TRH and VIP were similar to those in freshly dispersed cells with respect to PRL release, whereas those of GRF and SRIF were less potent with respect to GH release. The stimulation of GH and PRL release in P0 cells by adenylate cyclase-related agents ((Bu)2 cAMP and forskolin) was comparable to that for GH secretion in mature somatotrophs but much greater than that of PRL release in mature lactotrophs. Stimulation of GH and PRL release in P0 cells by protein kinase C-related agents (diacylglycerol and phorbol ester) was also similar to that observed for GH release from mature pituitary cells, whereas minimal or undetectable effects were observed on PRL release from mature cells. The results indicate that the P0 somatomammotropic cell line possesses receptors, second messenger systems, and secretory characteristics of both somatotrophs and lactotrophs, although where differences exist, there is more resemblance to somatotrophs. They also demonstrate that the responses to each of the agents studied are bihormonal and appear to be regulated by a common mechanism.
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PMID:Growth hormone and prolactin secretion in cultured somatomammotroph cells. 197 45

This study tests the hypothesis that atrial natriuretic factor (ANF) and C-ANF(4-23)-NH2 (C-ANF) augment cGMP generation and inhibit both cAMP generation and depolarization-induced catecholamine release in nerve growth factor treated pheochromocytoma cells by a pertussis toxin (PTX)-sensitive mechanism. Synthetic rat ANF(99-126) and the clearance receptor antagonist C-ANF (10(-12)-10(-9) M) inhibited basal and 5 microM vasoactive intestinal peptide (VIP)-induced cAMP generation in a concentration-dependent manner. These actions of ANF and C-ANF were blocked by 12-18 h pretreatment with PTX (100 ng/ml), suggesting ANF receptor coupling to adenylate cyclase via an inhibitory guanine nucleotide-binding protein. Both ANF (10(-11)-10(-9) M) and C-ANF (10(-11)-10(-8) M) also inhibited K(+)-induced catecholamine release in a concentration-dependent manner. ANF (10(-11)-10(-8) M) increased cGMP generation in a concentration-dependent manner but C-ANF did not. The accumulation of cGMP in response to ANF was not altered by treatment with PTX. Therefore, PTX dissociated the increased concentrations of cGMP from the ANF-mediated depression of evoked catecholamine release. C-ANF also dissociated elevations in cGMP concentrations from an ANF-mediated attenuation of evoked catecholamine release. The results of this study indicate that ANF inhibits adrenergic neurotransmission independent of guanylate cyclase.
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PMID:Neuromodulatory effects of atrial natriuretic factor are independent of guanylate cyclase in adrenergic neuronal pheochromocytoma cells. 197 29

We characterized a new type of vasoactive intestinal peptide (VIP) receptors in the CD4+ Stanford University Pediatric (SUP)-T1 lymphoma cell line, by comparing receptor occupancy [in the presence of (125I)helodermin and (125I)(acetyl-His1)VIP] and adenylate cyclase activation (in the presence of GTP). The order of potency of peptides on both parameters was: helodermin greater than (acetyl-His1)VIP greater than (Phe1)VIP = VIP greater than PHI while secretin was ineffective. In membranes, when Gs was permanently activated by Gpp(NH)p or by ADP-ribosylation (after pretreating intact lymphoblasts for 2 h with cholera toxin), there resulted a variably increased affinity of receptors for VIP-like peptides, suggesting reduced receptor selectivity. Preexposing intact lymphoblasts to the same peptides induced, within 5 min, homologous desensitization (i.e. reduced binding capacity and even more so impaired capability to activate adenylate cyclase), whose extent correlated with the Kd of each peptide at time 0. After prolonged (16 h) exposure to 30 nM VIP that resulted in marked (75%) downregulation, 60% of the adenylate cyclase responsiveness could recover within 30-120 min even in the presence of cycloheximide, but further resensitization was cycloheximide-sensitive. To conclude, VIP receptors coupled to adenylate cyclase showed distinct specificity in human SUP-T1 lymphoblasts. Their specificity decreased when Gs was permanently activated. In intact cells exposed to VIP-like peptides, the receptors were rapidly desensitized, then down-regulated, the resensitization mechanism being not immediately inhibited by cycloheximide.
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PMID:VIP receptors in human SUP-T1 lymphoblasts. 197 77

The vasoactive intestinal peptide (VIP) has shown to be widely distributed in the gastrointestinal mucosa, submucosa and nerves, and the existence of VIP receptors on the basolateral membrane of enterocytes has been recently reported for many species. The interaction of VIP with its receptors seemed to increase cyclic AMP level, and this nucleotide has been shown to be responsible for the intestinal secretion produced by VIP. The present study confirms that VIP inhibits the intestinal absorption of D-galactose. This effect seems to be due to the inhibition of the Na(+)-independent basolateral intestinal sugar transport system. RMI 12330A, described as adenylate cyclase inhibitors, blocked the VIP action. These findings suggest that cyclic AMP might be responsible for the inhibition of Na(+)-independent transport of D-galactose across the basolateral membrane. Moreover, results obtained to determine the possible role of calcium in the action of VIP suggest that Ca2+ play a part, directly or indirectly, in the inhibition of the D-galactose transport across the basolateral membrane produced by VIP.
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PMID:Effect of VIP on sugar transport in rabbit small intestine in vitro. 211 49

Receptor-mediated regulation of the sodium-phosphate symporter, and hence sodium-dependent phosphate uptake, typically relates to epithelial cells of renal origin. In this study we have characterized sodium-dependent phosphate uptake and aspects of its receptor-mediated regulation in the HeLa cell line, a cell line derived from a human epithelioid carcinoma. Phosphate uptake (greater than 90% sodium dependent; Vmax = 4.02 +/- 0.24 nmol.mg and Km = 0.11 +/- 0.02 mM phosphate at 140 mM sodium) was kinetically similar to that observed in opossum kidney cells. Incubation with vasoactive intestinal peptide (VIP) resulted in a dose-dependent (50% maximal dose of 8.8 +/- 3.6 nM) approximately fivefold increase in basal adenosine 3',5'-cyclic monophosphate (cAMP) levels (basal = 14.6 +/- 1.7 pmol.mg protein-1.15 min-1; VIP stimulated = 72.7 +/- 13.2 pmol.mg protein-1.15 min-1), as well as a dose-dependent maximal 32.6 +/- 5.5% decrease in sodium-dependent phosphate uptake (50% maximal decrease of 46.2 +/- 21.2 nM). The VIP-induced decrease in phosphate uptake was due to decrease in maximal transport (VmaxVIP = 2.78 +/- 0.16 nmol.mg protein-1.3 min-1) and not to a change in the affinity of the transporter for phosphate (KmVIP = 0.11 +/- 0.01 mM phosphate). Preincubation of HeLa cells with forskolin and cholera toxin, which stimulate adenylate cyclase, resulted in dose-dependent decreases in sodium-dependent phosphate uptake. Incubation with 8-bromo-cAMP and dibutyryl cAMP, permeant analogues of cAMP, similarly resulted in a dose-dependent decrease in sodium-dependent phosphate uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HeLa cells express cAMP-inhibitable sodium-dependent phosphate uptake. 215 43

We characterized highly selective receptors for PACAP, the pituitary adenylate cyclase activating peptide, in the tumoral acinar cell line AR 4-2J derived from the rat pancreas. PACAP, a novel hypothalamic peptide related to vasoactive intestinal peptide (VIP), was tested as the full natural 38-residue peptide (PACAP-38) and as an N-terminal amidated 27-residue derivative (PACAP-27). The binding sites showed considerable affinity for [125I]PACAP-27 (Kd = 0.4 nM) and PACAP-38, while their affinity for VIP and the parent peptide helodermin was 1000-fold lower. These receptors were coupled to adenylate cyclase, the potency of PACAP-38 and PACAP-27 (Kact = 0.2 nM) being much higher than that of VIP (Kact = 100 nM) and helodermin (Kact = 30 nM). Chemical cross-linking of [125I]PACAP-27 followed by SDS-PAGE and autoradiography revealed a specifically cross-linked peptide with an Mr of 68,000 (including 3000 for one PACAP-27 molecule).
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PMID:Presence of highly selective receptors for PACAP (pituitary adenylate cyclase activating peptide) in membranes from the rat pancreatic acinar cell line AR 4-2J. 215 35

The effect of vasoactive intestinal peptide (VIP) on prolactin (PRL) secretion from pituitary cells is reviewed and compared to the effect of thyrotropin releasing hormone (TRH). These two peptides induced different secretion profiles from parafused lactotrophs in culture. TRH was found to increase PRL secretion within 4 s and induced a biphasic secretion pattern, while VIP induced a monophasic secretion pattern after a lag time of 45-60 s. The secretion profiles are compared to changes in adenylate cyclase activity, production of inositol polyphosphates, changes in intracellular calcium concentrations and changes in electrophysiological properties of the cell membrane.
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PMID:The mechanisms by which vasoactive intestinal peptide (VIP) and thyrotropin releasing hormone (TRH) stimulate prolactin release from pituitary cells. 216 2

Specific binding of 125I-labelled GLP-1(7-36)amide to rat lung membranes was dependent upon time and temperature and was proportional to membrane protein concentration. Binding was inhibited in a concentration-dependent manner by unlabelled GLP-1(7-36)amide consistent with the presence of a single class of binding sites with a dissociation constant (Kd) of 1.67 +/- 0.29 nmol/l. GLP-1(1-36)amide was 260 times less potent in inhibiting the binding of 125I-labelled GLP-1(7-36)amide to lung membranes (Kd of 448 +/- 93 nmol/l). Vasoactive intestinal polypeptide and peptide-histidine-isoleucine also displaced 125I-labelled GLP-1(7-36)amide from the receptor concentration-dependently; the Kd was 4.31 +/- 0.8 and 7.93 +/- 4.79 nmol/l, respectively. Guanine nucleotides (GTP-gamma-S, GDP-beta-S) decreased the binding of 125I-labelled GLP-1(7-36)amide to rat lung membranes as was found for GLP-1(7-36)amide receptors in RINm5F cells which were also shown to be coupled to the adenylate cyclase system.
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PMID:Characterization of receptors for glucagon-like peptide-1(7-36)amide on rat lung membranes. 216 2

1. A direct action of vasoactive intestinal peptide (VIP) upon human kidney was sought by measurement of renal adenylate cyclase in tissue homogenates and plasma membranes isolated from tissue samples excised for therapeutic reasons. 2. VIP (1 microM) produced a mean stimulation of adenylate cyclase activity of 3.5-fold compared to basal values in cortical plasma membranes; comparative stimulations of 2.8-fold and 27.3-fold were obtained with 1 microM-glucagon and 1 microM-h(1-34) parathyroid hormone respectively. 3. Half-maximal stimulation of human renal cortical plasma membrane adenylate cyclase was observed with a mean value of 35 nM-VIP. 4. The stimulation of renal adenylate cyclase by VIP appeared to be specific because stimulation by glucagon was additive to that obtained with VIP, and the VIP receptor antagonist (4 Cl-D-Phe6, Leu17)-VIP inhibited the VIP-dependent stimulation of adenylate cyclase activity.
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PMID:Vasoactive intestinal peptide stimulation of human renal adenylate cyclase in vitro. 216 66

Afferent influences on natural cell death were modeled in retinal cultures derived from neonatal rats. Tetrodotoxin (TTX) blockade of electrical activity produced a significant reduction in surviving retinal ganglion cell (RGC) neurons during a critical period of development, similar in magnitude to the reduction observed during natural cell death in the intact retina at a similar developmental stage. The addition of vasoactive intestinal peptide (VIP) protected the RGCs from the lethal action of TTX. This effect was specific, since the related peptides PHI-27 and secretin produced no significant increase in RGC survival. Radioimmunoassay of cyclic nucleotides showed that TTX decreased culture levels of cAMP and that this trend was reversed by VIP. Decreases in RGC survival associated with TTX electrical blockade were prevented by 8-bromo:cAMP or forskolin. Furthermore, VIP10-28, the C-terminal fragment that inhibits VIP stimulation of adenylate cyclase, reduced the number of surviving RGCs. Thus, our results suggest that VIP, acting by increasing cAMP, has a neurotrophic effect on electrically blocked RGCs and may be an endogenous factor modulating normal cell death in the retina.
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PMID:VIP-mediated increase in cAMP prevents tetrodotoxin-induced retinal ganglion cell death in vitro. 216 72


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