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TY - JOUR. T1 - Capsaicinoids regulate airway anion transporters through rho kinase- and cyclic AMP-dependent mechanisms. AU - Hibino, Yoshitaka. AU - Morise, Masahiro. AU - Ito, Yasushi. AU - Mizutani, Takefumi. AU - Matsuno, Tadakatsu. AU - Ito, Satoru. AU - Hashimoto, Naozumi. AU - Sato, Mitsuo. AU - Kondo, Masashi. AU - Imaizumi, Kazuyoshi. AU - Hasegawa, Yoshinori. PY - 2011/10/1. Y1 - 2011/10/1. N2 - To investigate the effects of capsaicinoids on airway anion transporters, we recorded and analyzed transepithelial currents in human airway epithelial Calu-3 cells. Application of capsaicin (100 μM) attenuated vectorial anion transport, estimated as short-circuit currents (I SC), before and after stimulation by forskolin (10 μM) with concomitant reduction of cytosolic cyclic AMP (cAMP) levels. The capsaicin-induced inhibition of I SC was also observed in the response to 8-bromo-cAMP (1 mM, a cell-permeable cAMP analog) and 3-isobutyl-1-methylxanthine (1 mM, an inhibitor of ...
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BioAssay record AID 720707 submitted by NCGC: qHTS for Agonist of cAMP-regulated guanine nucleotide exchange factor 3 (EPAC1): primary screen.
Looking for online definition of cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) in the Medical Dictionary? cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) explanation free. What is cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP)? Meaning of cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) medical term. What does cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) mean?
The subcellular distribution of protein kinase activity in isolated islets of Langerhans was determined. The majority (70%) of cyclic AMP-dependent protein kinase activity was located in the S-100 (soluble) fraction, while the majority (42%) of cyclic AMP-independent activity was located in the solublised P-100 (containing mitochondria, secretory granules and microsomes) fraction. Partial characterisation of the islet cyclic AMP-dependent protein kinase activity revealed the presence of two isozymes designated Type I and Type II. Type II kinase was the predominant isozyme of the S-100 fraction and Type I was the predominant isozyme found in the solublised P-100 fraction. Nonidet-P40 (a non-ionic detergent) was found to activate the S-100 cyclic AMP-dependent protein kinase activity, although no significant increase in protein kinase activity was observed when the P-0.6 (containing nuclei and cellular debris) fraction and P-100 fraction were solublised with Nonidet-P40. This activation was ...
Phototaxis and thermotaxis by Dictyostelium discoideum slugs on water agar were impaired by the presence in the agar of adenosine, which is a cyclic AMP receptor antagonist in aggregating amoebae. Caffeine, and presumably its analogue theophylline, inhibit cyclic AMP signalling in aggregating amoebae of D. discoideum. Both compounds perturbed slug behaviour in a similar manner to adenosine, as did both ammonium and sulphate ions. (NH4)3SO4 is known to perturb cyclic AMP binding to its receptor, and ammonia is an inhibitor of cyclic AMP signalling in aggregating amoebae. The receptor agonist, cyclic AMPS, disrupted slug organization and impaired phototaxis when present at concentrations high enough to saturate cyclic AMP receptors and compete effectively with endogenous cyclic AMP signals of similar magnitude to those observed during aggregation. Taken together with the considerable circumstantial evidence for cyclic AMP signalling in slugs, these results support a role for cyclic AMP signalling ...
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The mechanisms by which adenosine triphosphate, thrombin, and trypsin cause relaxation of vascular smooth muscle were investigated. Relaxation of the rat thoracic aorta with adenosine triphosphate, thrombin, and/or trypsin was associated with increased levels of cyclic guanosine monophosphate in both time- and concentration-dependent manners. Thrombin and trypsin did not alter cyclic adenosine monophosphate levels, whereas adenosine triphosphate increased cyclic adenosine monophosphate levels after significant relaxation occurred. Removal of the endothelium abolished adenosine triphosphate-, thrombin-, and trypsin-induced relaxation and the associated increased levels of cyclic nucleotides. Relaxation due to these agents was also inhibited by exposure to nordihydroguaiaretic acid, a lipoxygenase inhibitor, and eicosatetraynoic acid, a lipoxygenase and cyclooxygenase inhibitor. Indomethacin, a cyclooxygenase inhibitor, potentiated relaxation to these agents, whereas the increased levels of cyclic ...
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By differential hybridization, we identified a number of genes in Saccharomyces cerevisiae that are activated by addition of cyclic AMP (cAMP) to cAMP-depleted cells. A majority, but not all, of these genes encode ribosomal proteins. While expression of these genes is also induced by addition of the appropriate nutrient to cells starved for a nitrogen source or for a sulfur source, the pathway for nutrient activation of ribosomal protein gene transcription is distinct from that of cAMP activation: (i) cAMP-mediated transcriptional activation was blocked by prior addition of an inhibitor of protein synthesis whereas nutrient-mediated activation was not, and (ii) cAMP-mediated induction of expression occurred through transcriptional activation whereas nutrient-mediated induction was predominantly a posttranscriptional response. Transcriptional activation of the ribosomal protein gene RPL16A by cAMP is mediated through a upstream activation sequence element consisting of a pair of RAP1 binding ...
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Bradykinin and phorbol 12-myristate 13-acetate stimulate adenylate cyclase activity in serum-depleted cultured airway smooth muscle via a protein kinase C (PKC)-dependent pathway. The probable target is the type II adenylate cyclase, which can integrate coincident signals from both PKC and Gs. Therefore, activation of Gs (by cholera-toxin pre-treatment) amplified the bradykinin-stimulated cyclic AMP signal and concurrently attenuated the partial activation of extracellular-signal-regulated kinase-2 (ERK-2) by bradykinin. We have previously demonstrated that, in order to induce full activation of ERK-2 with bradykinin, it is necessary to obliterate PKC-stimulated cyclic AMP formation. We concluded that the cyclic AMP signal limits the magnitude of ERK-2 activation [Pyne, Moughal, Stevens, Tolan and Pyne (1994) Biochem. J. 304, 611-616]. The present study indicates that the bradykinin-stimulated ERK-2 pathway is entirely cyclic AMP-sensitive, and suggests that coincident signal detection by ...
TY - JOUR. T1 - Immunocytochemical expression of human muscle cell p75 neurotrophin receptor is down-regulated by cyclic adenosine 3,5-monophosphate. AU - Baron, Pierluigi. AU - Scarpini, Elio. AU - Pizzul, Silvia. AU - Zotti, Fabrizio. AU - Conti, Giancarlo. AU - Pleasure, David E. AU - Scarlato, Guglielmo. PY - 1997/10/3. Y1 - 1997/10/3. N2 - To investigate whether the immunocytochemical expression of low affinity neurotrophin receptor (p75) in human muscle is modulated by increased levels of intracellular cyclic adenosine 3,5-monophoshate (cAMP), human cultured myogenic cells were treated with cAMP analogues dibutyryl cAMP (dbcAMP 0.5-1 mM) and 8-bromo cAMP (1 mM) or the adenylate cyclase activator forskolin (10- 100 μM). Cultures were processed for indirect immunofluorescence microscopy using an anti-human p75 mAb. The treatment of cultured muscle cells with cAMP analogues or forskolin for two days induced a decrease of immunoreactivity for p75 and a reduction of both myotube formation ...
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An antiserum against the catalytic subunit C of cyclic AMP-dependent protein kinase, isolated from bovine heart type II protein kinase, was produced in rabbits. Reaction of the catalytic subunit with antiserum and separation of the immunoglobulin G fraction by Protein A-Sepharose quantitatively removed the enzyme from solutions. Comparative immunotitration of protein kinases showed that the amount of antiserum required to eliminate 50% of the enzymic activity was identical for pure catalytic subunit, and for holoenzymes type I and type II. The reactivity of the holoenzymes with the antiserum was identical in the absence or the presence of dissociating concentrations of cyclic AMP. Most of the holoenzyme (type II) remains intact when bound to the antibodies as shown by quantification of the regulatory subunit in the supernatant of the immunoprecipitate. Titration with the antibodies also revealed the presence of a cyclic AMP-independent histone kinase in bovine heart protein kinase I preparations ...
The regulatory subunits of protein kinase A, or cyclic AMP-binding proteins, were measured in a series of 107 human ovarian tumors (89 malignant, 7 borderline, and 11 benign tumors) and related to tumor clinicopathological features and patient survival. Total cyclic AMP-binding protein levels were not significantly different between malignant tumors and either borderline or benign tumors. However, serous tumors showed significantly higher levels of total cyclic AMP-binding proteins than other malignant tumors (P = 0.007). Poorly differentiated tumors also possessed significantly higher levels of binding proteins as compared with well/moderately differentiated tumors (P , 0.01). Retrospective analysis of follow-up data also revealed a significant trend for patients with high tumor cyclic AMP-binding proteins to have poorer survival (P = 0.03). Individual binding proteins were identified by photoaffinity labeling, and the RI (Mr 48,000) protein was expressed as a percentage of total cyclic ...
Tisdale, M J. and Phillips, B J., Apparent correlation between adenosine 3.5 Cyclic monophosphate levels and malignancy in somatic cell hybrids. (1974). Subject Strain Bibliography 1974. 1875 ...
Looking for online definition of cyclic AMP, 3',5'-cAMP in the Medical Dictionary? cyclic AMP, 3',5'-cAMP explanation free. What is cyclic AMP, 3',5'-cAMP? Meaning of cyclic AMP, 3',5'-cAMP medical term. What does cyclic AMP, 3',5'-cAMP mean?
One of the most promising new targets for trypanocidal drugs to emerge in recent years is the cyclic AMP (cAMP) phosphodiesterase (PDE) activity encoded by TbrPDEB1 and TbrPDEB2. These genes were genetically confirmed as essential, and a high-affinity inhibitor, CpdA, displays potent antitrypanosomal activity. To identify effectors of the elevated cAMP levels resulting from CpdA action and, consequently, potential sites for adaptations giving resistance to PDE inhibitors, resistance to the drug was induced. Selection of mutagenized trypanosomes resulted in resistance to CpdA as well as cross-resistance to membrane-permeable cAMP analogues but not to currently used trypanocidal drugs. Resistance was not due to changes in cAMP levels or in PDEB genes. A second approach, a genome-wide RNA interference (RNAi) library screen, returned four genes giving resistance to CpdA upon knockdown. Validation by independent RNAi strategies confirmed resistance to CpdA and suggested a role for the identified cAMP ...
Specificity and versatility in cAMP signalling are governed by the spatial localization and temporal dynamics of the signal. Phosphodiesterases (PDEs) are important for shaping cAMP signals by hydrolyzing the nucleotide. In pancreatic β-cells, glucose triggers sub-plasma membrane cAMP oscillations important for insulin secretion, but the mechanisms underlying the oscillations are poorly understood. Here, we investigated the role of different PDEs for generating cAMP oscillations by monitoring the sub-membrane cAMP concentration ([cAMP]pm) with ratiometric evanescent wave microscopy in MIN6-cells or mouse pancreatic β-cells expressing a fluorescent translocation biosensor. The general PDE inhibitor IBMX increased [cAMP]pm, and while oscillations were frequently observed at 50 µM IBMX, 300 µM-1 mM of the inhibitor caused stable [cAMP]pm elevation. [cAMP]pm was nevertheless markedly suppressed by the adenylyl cyclase inhibitor 2′,5′-dideoxyadenosine, indicating also IBMX-insensitive cAMP ...
We demonstrate that JunD, a component of the AP-1 transcription factor complex, activates transcription of the human proenkephalin gene in a fashion that is completely dependent upon the cAMP-dependent protein kinase, protein kinase A. Activation of proenkephalin transcription by JunD is dependent upon a previously characterized cAMP-, phorbol ester-, and Ca(2+)-inducible enhancer, and JunD is shown to bind the enhancer as a homodimer. Another component of the AP-1 transcription complex, JunB, is shown to inhibit activation mediated by JunD. As a homodimer JunB is unable to bind the enhancer; however in the presence of c-Fos, high-affinity binding is observed. Furthermore, JunD is shown to activate transcription of genes linked to both cAMP and phorbol ester response elements in a protein kinase A-dependent fashion, further blurring the distinction between these response elements. These results demonstrate that the transcriptional activity of an AP-1-related protein is regulated by the ...
The LNCaP cell line is a versatile and useful model that is suitable for the study of human prostate cancer in vitro. The elevation of LNCaP intracellular cAMP levels through the addition of membrane permeable cAMP analogues, phosphodiesterase inhibitors, adenylate cyclase activators, or components of the cAMP signal transduction pathway can induce reversible neuroendocrine differentiation. Elucidation of those genes that are differentially expressed between undifferentiated prostate cancer cells and prostate cancer cells that have been induced to differentiate may present new insights for the molecular mechanisms governing neuroendocrine differentiation, early detection of prostate cancer, and/or potential targets for gene therapy. In this study, differential display PCR was used to identify 226 differentially expressed PCR products. Twelve of the differential display PCR products were confirmed by Northern blot analysis and cloned. DNA sequencing and database comparisons were performed. Among ...
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Nine membrane-bound adenylyl cyclase isoforms catalyze the production of the second messenger cyclic AMPs (cAMP) in response to various stimuli. Reduction of adenylyl cyclase activity has well-documented benefits, including for heart disease and pain. These roles have inspired an attempt to develop isoform selective adenylyl cyclase inhibitors. The lack of true selectivity currently limits exploration of functions and/or treatment of dysfunctions involving adenylyl cyclase/cAMP signaling. The present study demonstrated that a panel of inhibitors described as AC5-selective actually does not discriminate between AC5 and AC6. Likewise, the putative AC1-selective inhibitor, NB001 [5-[[2-(6-amino-9H-purin-9-yl)ethyl]amino]-1-pentanol], does not directly target AC1 to reduce cAMP levels. These results lead to a discussion regarding the need to reinterpret literature using AC5/6-selective molecules.. See article at J Pharmacol Exp Ther 2013, 347:265-275.. ...
Werner, C.G., Godrey, V., Arnold, R.R., Featherstone, G.L., Bender, D., Schlossmann, Jens, Schiemann, M., Hofmann, F. and Pryzwansky, K.B. (2005) Neutrophil dysfunction in guanosine 3,5-cyclic monophosphate-dependent protein kinase I-deficient mice. Journal of Immunology 175, pp. 1919-1929 ...
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H2O2 and oxygen-derived free radicals modulate vasodilator mechanisms.1 2 3 4 5 6 9 The present studies indicate that H2O2 enhances adenylyl cyclase activation and that the effect is dependent (in part) on the presence of iron and is blunted by agents that act to inhibit tyrosine kinase activity.. Our data suggest that the oxygen-derived species mediating the enhancement of adenylyl cyclase activation is either H2O2 itself or the hydroxyl radical. Incubation of cells with xanthine oxidase and purine resulted in a qualitatively similar enhancement of adenylyl cyclase activation. The effect of purine and xanthine oxidase was not blocked by coincubation with superoxide dismutase (which catalyzes the conversion from superoxide anion to H2O2). This suggests that the generation of the superoxide anion is not involved in the mechanism of enhancement of adenylyl cyclase activation. However, pretreatment with either catalase (which catalyzes conversion of H2O2 to water) or with deferoxamine (which ...
Recent evidence suggests that ethanol initially causes an increase in receptor-dependent cAMP levels, followed by heterologous desensitization of receptors coupled to GS after chronic exposure. Here we investigated the role of adenosine in mediating these responses. We found that ethanol caused accumulation of extracellular adenosine in NG108-15 and S49 lymphoma cells. This adenosine activated adenosine receptors to increase intracellular cAMP levels. The addition of adenosine deaminase, to degrade accumulated extracellular adenosine, or isobutyl-methylxanthine, an adenosine receptor antagonist, completely blocked ethanol-induced increases in cAMP levels in NG108-15 cells. Chronic exposure of NG108-15 and S49 wild type cells to ethanol resulted in heterologous desensitization of adenosine receptor- and prostaglandin E1 receptor-dependent cAMP signal transduction. Coincubation of NG108-15 and S49 wild type cells with adenosine deaminase and ethanol for 48 hr prevented heterologous ...
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TY - JOUR. T1 - Phosphodiesterase III Inhibition Increases cAMP levels and augments the infarct size limiting effect of a dpp-4 inhibitor in mice with type-2 diabetes mellitus. AU - Birnbaum, Yochai. AU - Castillo, Alexander C.. AU - Qian, Jinqiao. AU - Ling, Shukuan. AU - Ye, Hongmei. AU - Perez-Polo, Jose R.. AU - Bajaj, Mandeep. AU - Ye, Yumei. PY - 2012/12/1. Y1 - 2012/12/1. N2 - Purpose We assessed whether phosphodiesterase-III inhibition with cilostazol (Cil) augments the infarct size (IS)-limiting effects of MK0626 (MK), a dipeptidyl-peptidase-4 (DPP4) inhibitor, by increasing intracellular cAMP in mice with type-2 diabetes. Methods Db/Db mice received 3-day MK (0, 1, 2 or 3 mg/kg/d) with or without Cil (15 mg/kg/d) by oral gavage and were subjected to 30 min coronary artery occlusion and 24 h reperfusion. Results Cil and MK at 2 and 3 mg/kg/d significantly reduced IS. Cil and MK had additive effects at all three MK doses. IS was the smallest in the MK-3+Cil. MK in a dose dependent manner ...
Adenylyl Cyclase Type V Inhibitor, NKY80 - CAS 299442-43-6 - Calbiochem The Adenylyl Cyclase Type V Inhibitor, NKY80, also referenced under CAS 299442-43-6, controls the biological activity of Adenylyl Cyclase Type V. This small molecule/inhibitor is primarily used for Cell Signaling applications. - Find MSDS or SDS, a COA, data sheets and more information.
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In Schwann cells (SCs), cyclic adenosine monophosphate (cAMP) not only induces differentiation into a myelinating SC-related phenotype, but also synergistically enhances the mitogenic action of growth factors such as neuregulin. impairment of SC differentiation and myelin formation but not Krox-20 expression, which indicates an independent mechanism of Krox-20 regulation in response to cAMP. In conclusion, our data supports the idea that the outcome of cAMP signaling in SCs depends on the particular set of effectors activated. Whereas the mitogenic action of cAMP relies exclusively on PKA activity, the differentiating action of cAMP requires a PKA-independent (non-canonical) cAMP-specific pathway that is partially transduced by EPAC. Introduction The ubiquitous second messenger cyclic adenosine monophosphate (cAMP) is usually a key regulator of metabolic activity, survival, proliferation and differentiation in a wide variety of cell types. In particular, isolated cultured Schwann cells (SCs), ...
Psoriasis is a chronic, systemic, inflammatory disease with manifestations resulting from a dysregulated immune response. In psoriatic skin, expression of all phosphodiesterase 4 (PDE4) isoforms (A-D), part of a family of enzymes known to regulate cyclic adenosine monophosphate levels and immune homeostasis, is elevated compared with healthy controls. Agents that inhibit the enzymatic activity of PDE4, the predominant PDE in most immune cells, exert well-recognized anti-inflammatory effects. Apremilast is a selective PDE4 inhibitor approved for the treatment of adults with moderate to severe plaque psoriasis and/or psoriatic arthritis. In vitro and in vivo investigations have demonstrated the beneficial impact of apremilast treatment on PDE4 activity, inflammatory signal expression, and dermal psoriasiform signs. In patients with moderate to severe psoriasis, treatment with apremilast is associated with significant reductions in plasma levels of interleukin (IL)-17F, IL-17A, IL-22, and tumor necrosis
Desensitization is defined as a decreased functional response after continuous or repetitive stimulation of a receptor with its agonist. Thyrotropin (TSH) increases cAMP levels in normal and neoplastic thyroid tissue. The tumor promoter 12-O-tetradecanogl-phorbol-13-acetate (TPA) activates protein kinase C (PKC). The aim was to determine whether TPA induces heterologous desensitization of the TSM-adenylate cyclase (AC) signal transduction system, Three human thyroid neoplasms in culture for 6 months or longer tone papillary carcinoma, one Hurthle cell carcinoma, one follicular adenoma) were incubated with TSH (10 mU/ml) and TPA (1.6 x 10(-8) M) separately and together for various time periods (from 10 minutes to 24 hours). The mixture mas subsequently incubated for 30 minutes with TSH. TPA alone had no effect on cAMP Levels, but co-incubation of TPA and TSH caused a significant reduction in cAMP response when compared to the cAMP response that resulted after stimulation with only TSH (p < ...