Academic literature on the topic 'Cyclic guanosine 3',5'-monophosphate'

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Journal articles on the topic "Cyclic guanosine 3',5'-monophosphate"

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Srivastava, Uma S., Manohar Lal Thakur, and C. Spach. "Cyclic 3′, 5′-adenosine monophosphate and cyclic 3′, 5′-guanosine monophosphate metabolism in malnutrition." Nutrition Research 6, no. 5 (May 1986): 589–99. http://dx.doi.org/10.1016/s0271-5317(86)80113-0.

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Boadu, Emmanuel, Svanhild Vaskinn, Elisabeth Sundkvist, Ragnhild Jaeger, and Georg Sager. "Inhibition by guanosine cyclic monophosphate (cGMP) analogues of uptake of [3H]3′,5′-cGMP without stimulation of ATPase activity in human erythrocyte inside-out vesicles11Abbreviations: 3′,5′-cGMP, guanosine 3′,5′-cyclic monophosphate; 2′,3′-cGMP, guanosine 2′,3′-cyclic monophosphate; N-mb-cGMP, N2-monobutyryl guanosine 3′,5′-cyclic monophosphate; O-mb-cGMP, 2′-O-monobutyryl guanosine 3′,5′-cyclic monophosphate; Db-cGMP, N2,2′-O-dibutyryl guanosine 3′,5′-cyclic monophosphate; Br-cGMP, 8′-bromo guanosine 3′,5′-cyclic monophosphate; Rp-cGMPS, Rp-monophosphorothioate guanosine 3′,5′-cyclic monophosphate; Sp-cGMPS, Sp-monophosphorothioate guanosine 3′,5′-cyclic monophosphate; 3′,5′-cAMP, Adenosine 3′,5′-cyclic monophosphate; and MRP, multidrug resistance protein." Biochemical Pharmacology 62, no. 4 (August 2001): 425–29. http://dx.doi.org/10.1016/s0006-2952(01)00682-7.

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Pradelles, Philippe, Jacques Grassi, Danielle Chabardes, and Nicole Guiso. "Enzyme immunoassays of adenosine cyclic 3',5'-monophosphate and guanosine cyclic 3',5'-monophosphate using acetylcholinesterase." Analytical Chemistry 61, no. 5 (March 1989): 447–53. http://dx.doi.org/10.1021/ac00180a014.

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Beste, Kerstin Y., and Roland Seifert. "cCMP, cUMP, cTMP, cIMP and cXMP as possible second messengers: Development of a hypothesis based on studies with soluble guanylyl cyclase α1β1." Biological Chemistry 394, no. 2 (February 1, 2013): 261–70. http://dx.doi.org/10.1515/hsz-2012-0282.

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Abstract Adenosine 3′,5′-cyclic monophosphate and guanosine 3′,5′-cyclic monophosphate are second messengers that regulate multiple physiological functions. The existence of additional cyclic nucleotides in mammalian cells was postulated many years ago, but technical problems hampered development of the field. Using highly specific and sensitive mass spectrometry methods, soluble guanylyl cyclase has recently been shown to catalyze the formation of several cyclic nucleotides in vitro. This minireview discusses the broad substrate-specificity of soluble guanylyl cyclase and the possible second messenger roles of cyclic nucleotides other than adenosine 3′,5′-cyclic monophosphate and guanosine 3′,5′-cyclic monophosphate. We hope that this article stimulates productive and critical research in an area that has been neglected for many years.
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Meskini, N., O. MacOvschi, A. F. Prigent, G. Nemoz, P. Chapuy, and M. Lagarde. "Decreased Cyclic Nucleotide Phosphodiesterase Activity in Human Peripheral Blood Mononuclear Cells from Elderly Women." Clinical Science 79, no. 5 (November 1, 1990): 467–70. http://dx.doi.org/10.1042/cs0790467.

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1. Both adenosine 3′:5′-cyclic monophosphate and guanosine 3′:5′-cyclic monophosphate phosphodiesterase activities of peripheral blood mononuclear cells were markedly decreased in elderly women as compared with young control women. 2. In contrast, the ability of these cells to bind guanosine 5′-[β, γ-imido]triphosphate, a non-hydrolysable analogue of guanosine 5′-triphosphate, was the same in both groups. 3. These findings are discussed in the context of the decline in immune function which occurs with increasing age.
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Mattana, J., and P. C. Singhal. "Effects of atrial natriuretic peptide and cGMP on uptake of IgG complexes by macrophages." American Journal of Physiology-Cell Physiology 265, no. 1 (July 1, 1993): C92—C98. http://dx.doi.org/10.1152/ajpcell.1993.265.1.c92.

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Macromolecular handling by macrophages and glomerular mesangial cells may be important in the development of renal injury. We undertook the present study to determine whether atrial natriuretic peptide (ANP), a particulate guanylate cyclase stimulator, plays a direct role in uptake of immunoglobulin G (IgG) complexes by macrophages. Macrophages incubated with ANP at 10(-5) and 10(-6) M showed significantly suppressed uptake of IgG complexes compared with control. Macrophage uptake of IgG complexes was also significantly suppressed by the soluble guanylate cyclase stimulator sodium nitroprusside. Dibutyryl guanosine 3',5'-cyclic monophosphate and dibutyryl adenosine 3',5'-cyclic monophosphate both significantly suppressed IgG complex uptake as well. ANP was found to significantly enhance macrophage guanosine 3',5'-cyclic monophosphate (cGMP) levels compared with control cells, and this effect was antagonized by angiotensin II. Angiotensin II significantly enhanced uptake of IgG complexes and suppressed macrophage adenosine 3',5'-cyclic monophosphate synthesis, and both effects were antagonized by coincubation with ANP. These results suggest that ANP modulates uptake of IgG complexes by macrophages and that this effect may be mediated via cGMP.
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Géigel, LF, and LL Leon. "Cyclic 3'-5' guanosine monophosphate-dependent activity in Leishmania amazonensis." Memórias do Instituto Oswaldo Cruz 98, no. 4 (June 2003): 499–500. http://dx.doi.org/10.1590/s0074-02762003000400012.

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Santy, L. C., and G. Guidotti. "Reconstitution and characterization of two forms of cyclic nucleotide-gated channels from skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 271, no. 6 (December 1, 1996): E1051—E1060. http://dx.doi.org/10.1152/ajpendo.1996.271.6.e1051.

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A cyclic nucleotide-gated channel present in skeletal muscle plasma membrane has previously been identified as being responsible for insulin-activated sodium entry into muscle cells (J. E. M. McGeoch and G. Guidotti. J. Biol. Chem. 267:832-841, 1992). We have isolated this channel activity to further study and characterize it. The channel was solubilized from rabbit skeletal muscle sarcolemma and functionally reconstituted into phospholipid vesicles, as assayed by patch-clamp analysis of the reconstituted proteins. Channel activity was isolated by 8-bromo-guanosine 3',5'-cyclic monophosphate affinity chromatography, producing two distinct peaks of cyclic nucleotide-gated channel activity. These two types of channel activity differ in guanosine 3',5'-cyclic monophosphate affinity and in the ability to be opened by adenosine 3',5'-cyclic monophosphate. The cyclic nucleotide-gated channel from rod outer segments also forms two peaks of activity when purified in this manner. The presence of two forms of channel activity could have implications for the mechanism of insulin-activated sodium entry.
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Chen, Da-Chung, Shyng-Shiou F. Yuan, Her-Young Su, Shin-Chieh Lo, Shin-Sia Ren, and Gwo-Jang Wu. "Urinary cyclic guanosine 3′,5′-monophosphate and cyclic adenosine 3′,5′-monophosphate changes in spontaneous and induced onset active labor." Acta Obstetricia et Gynecologica Scandinavica 84, no. 11 (October 17, 2005): 1081–86. http://dx.doi.org/10.1111/j.0001-6349.2005.00831.x.

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Horton, J. K., R. C. Martin, S. Kalinka, A. Cushing, J. P. Kitcher, M. J. O'Sullivan, and P. M. Baxendale. "Enzyme immunoassays for the estimation of adenosine 3',5'cyclic monophosphate and guanosine 3',5'cyclic monophosphate in biological fluids." Journal of Pharmacological and Toxicological Methods 29, no. 4 (August 1993): 234. http://dx.doi.org/10.1016/1056-8719(93)90032-a.

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Dissertations / Theses on the topic "Cyclic guanosine 3',5'-monophosphate"

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Sriraman, R. "Cyclic guanosine 3', 5' - cyclic monophosphate (cGMP) enhancement & its relationship to vascular function & insulin sensitivity." Thesis, Exeter and Plymouth Peninsula Medical School, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701082.

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Li, Ying 1972 Mar 31. "The effects of cyclic guanosine 3', 5'-monophosphate analog on protein accumulation in adult rat cardiomyocytes in vitro /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101863.

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Cyclic guanosine 3', 5'-monophosphate (cGMP) has recently emerged as an endogenous regulator for controlling or reversing cardiac hypertrophy. Increased protein accumulation is a key feature of cardiac hypertrophy; thus, our study investigates the effects of a cGMP analog on protein accumulation in primary culture of adult rat cardiomyocytes and dissects out the mechanisms involved. We confirmed that a cGMP analog, 8-bromo-cGMP, inhibits phenylephrine (PE)-increased accumulation of newly synthesized proteins in cultured adult rat ventricular cardiomyocytes. Firstly, we have obtained data showing that 8-bromo-cGMP does not inhibit phosphorylation of S6K1 by PE during short time treatment (10 min to 2 h), but blocks phosphorylation of S6K1 by PE at 6 h; moreover this blocking effect is completely abolished by phosphatase inhibitor Tautomycin. Then, we have demonstrated that PE and cGMP induce sustained and transient increased phosphorylation of ERK, respectively. Moreover, cGMP inhibits PE-induced phosphorylation of ERK during long term treatment (3 and 6h). We have also shown that 8-bromo-cGMP inhibits ROS generation induced by PE. Other effects of PE that could be related to hypertrophy (i.e. increased concentration of upstream binding factor mRNA and decreased concentration of the mRNAs of Atrogin and muscle specific RING finger) were not abolished by 8-bromo-cGMP. We conclude that cGMP analog blocks protein accumulation by inhibiting the sustained phosphorylation of S6K1 via the activation of phosphatases.
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Hamad, Ahmed El-Sayed Mansour Abd El-Mohsen. "Guanosine 3': 5'-cyclic monophosphate regulation in cultured human airway smooth muscle cells and its role in proliferation." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298959.

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Cardoso, Andrea Rodrigues. "Mapeamento global de interações proteicas nas vias de sinalização mediadas por c-di-GMP de Pseudomonas aeruginosa." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/76/76132/tde-17052016-094656/.

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A persistência bacteriana correlacionada à formação de biofilmes bacterianos é, há algum tempo, fonte de grande preocupação médica em virtude de sua ampla associação com a dificuldade de tratamento de infecções crônicas. Por outro lado, as perspectivas de utilização de biofilmes bacterianos em novas aplicações biotecnológicas e até mesmo para fins terapêuticos são promissoras. Há, portanto, grande interesse em compreender os mecanismos que levam as células bacterianas a deixar o estado planctônico, de vida livre, e associarem-se nesses conglomerados celulares altamente complexos. Ao longo das últimas décadas, o segundo mensageiro c-di-GMP – em conjunto com as moléculas que catalisam sua síntese (diguanilato ciclases) e sua degradação (fosfodiesterases) e seus receptores – estabeleceu-se como um elemento central de regulação de uma série de respostas celulares que determinam a formação ou a dispersão de biofilmes. Curiosamente, as proteínas que participam do metabolismo deste segundo mensageiro estão, frequentemente, codificadas múltiplas vezes em um mesmo genoma bacteriano. Em vista dessa observação, estudos mais recentes apontam que, para reger paralelamente uma variedade tão ampla de fenótipos, este sistema opera em modo de alta especificidade de sinalização e que, portanto, o sinal metabolizado por determinados conjuntos de diguanilato ciclases e fosfodiesterases tem alvos celulares específicos. Evidências robustas, porém isoladas até o momento, apontaram que um dos meios pelo qual ocorre a segregação entre sinal produzido e alvo específico é a interação direta entre as proteínas componentes das vias de sinalização. Mais, demonstrou-se que, em algumas vias, a transmissão de sinal ocorre exclusivamente via interação proteica, dispensando a intermediação do sinalizador em si. Para avaliar a validade e relevância global deste mecanismo, propôs-se, neste estudo, a investigação da rede total de interações entre as proteínas tipicamente associadas às vias de sinalização por c-di-GMP em Pseudomonas aeruginosa, utilizando ensaios de duplo-hibrido bacteriano. Para tanto, foram construídas duas bibliotecas de DNA direcionadas e foram feitos testes de interação de forma estratégica para possibilitar o esgotamento e averiguação de todas as possíveis interações entre as proteínas alvo identificadas. O resultado obtido, um mapa inicial, porém abrangente, da rede de interações proteicas em P. aeruginosa, indica uma grande probabilidade de que os mecanismos previamente descritos sejam realmente recorrentes e relevantes para o intermédio da sinalização nesse organismo. Algumas das interações mais robustas encontradas são bastante interessantes e serão, em estudos futuros, mais extensivamente estudadas.
Persister bacteria are correlated to biofilm formation and have been a source of great medical concern due to its close association with the impairment of traditional treatment in combating chronic infections. On the other hand, using bacterial biofilms to create original biotechnological applications or even as a means of therapeutic treatment in medical settings constitutes a promising prospect. There is, therefore, a great interest in understanding the mechanisms that allow bacteria to leave the free-living planktonic lifestyle and associate in these highly complex cellular aggregates. Over the last decades, the second messenger c-di-GMP – and also the molecules involved in its synthesis (diguanylate ciclases) and degradation (phosphodiesterases) along with its receptors – has been established as a key element implicated in regulation of a series of cellular responses that determine biofilm formation or dispersion. Curiously, the proteins that play a part in the metabolism of this second messenger are frequently coded multiple times in single bacterial genomes. Taking this into account, recent studies indicate that, in order to control such a wide range of phenotypes, this system operates via high specificity of signaling – which means that the signal metabolized by a certain set of diguanylate ciclases and phosphodiesterases has specific cellular targets. Robust but yet isolated evidence indicate that a means by which a signal is segregated with its correlated phenotypic response is through direct protein-protein interaction involving the components of these signaling pathways. Even more, there has been strikingly evidence that, in some of these pathways, signal transduction occurs exclusively through protein-protein interaction, entirely dismissing any mediation by the signal molecule. In order to validate and evaluate the global relevance of this type of mechanism, this study proposed the investigation of the entire network of interactions between proteins typically associated with c-di-GMP signaling pathways of Pseudomonas aeruginosa by employing bacterial two-hybrid system assays. To make that possible, two DNA libraries were constructed and interaction essays were performed in a strategic way so that all possibilities of interaction between target proteins were explored. The results obtained from these experiments allowed the construction of a broad map of interactions that, although still primitive, indicates that, chances are, the mechanisms previously described are both recurrent and relevant to signaling regulation in this organism. Some of the interaction partners found are particularly interesting and will be further investigated in future studies.
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Jones, Christine. "Guanosine 5'-diphosphate 3'-diphosphate (ppGpp), guanosine 5'-diphosphate 3'-monophosphate (ppGp) and antibiotic production in Streptomyces clavuligerus." Thesis, University of Central Lancashire, 1996. http://clok.uclan.ac.uk/19767/.

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Streptomyces clavuligerus was grown in nutrient-limited defined media in laboratory scale fermenters using continuous and batch culture methods. Cephamycin C was produced in all fermentations. Clavulanic acid was produced in carbon- and nitrogenlimited continuous culture and in carbon- and phosphate-limited batch culture. Low levels of intracellular guanosine 5'-diphosphate 3'-diphosphate (ppGpp) were detected at D= 0.02 h' in continuous culture in all media. Low levels of intracellular guanosine 5 '-diphosphate 3 '-monophosphate (ppGp) were detected at D=0.02 if' in carbon- and nitrogen- limited media. ppop was not detected under phosphate limitation at any dilution rate. Increased production of cephamycin C was observed at D=0.02 If' under nitrogen limitation coinciding with the detection of elevated levels of ppGpp, ppGp and ATP. Increased production of clavulanic acid was observed at D=0.02 If' under carbon limitation coinciding with the detection of elevated levels of ppGpp and ppGp. There was no correlation between dilution rate and basal levels of either ppGpp or ppGp in any growth-limiting medium. ppGpp was produced at low levels in carbon- and nitrogen-limited batch fermentations prior to the detection of cephamycin C and clavulanic acid in the medium. High levels of ppGpp were detected under phosphate limitation immediately prior to the transcription of cas, the gene encoding clavaminate synthase. High levels of ppGp were detected in all batch fermentations following a downturn in nitrogen and carbon levels and immediately prior to the detection of isopenicillin N synthetase (IPNS). ppGp was detected following nutrient shifidown by amino acid depletion and was not produced via degradation of ppGpp. The results point to a possible role for ppGpp in the regulation of clavulanic acid synthesis under phosphate limitation only, and a potential role for ppGp in the regulation of cephamycin C production in Streptomyces clavuligerus.
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Bastani, A. "Biochemical study of cytidine 3',5' cyclic monophosphate phosphodiesterase activity." Thesis, Swansea University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.636051.

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Two enzymes capable of hydrolysing cytidine 3',5'-cyclic monophosphate have previously been reported, one (cCMP-specific PDE) with an absolute specificity for cCMP as substrate, and the other (multifunctional PDE) capable of hydrolysing a number of cyclic nucleotide substrates. This phosphodiesterase preparation was capable of hydrolysing different substrates (cyclic CMP > cyclic AMP > cyclic UMP > cyclic GMP) with the highest specific activity toward cyclic CMP as substrate. It was found to contain both the multifunctional and the cyclic CMP-specific phosphodiesterase, as shown by kinetic data, mass spectrometric analysis, and by utilizing isoelectric focusing and polyacrylamide gel electrophoresis. The PDE activity of the preparation was activated by cytidine and mercaptoethanol, inhibited by aspartate and arginine, but was insensitive to calmodulin. It was active in the absence of metal ions but inhibited by addition of Fe2+ and Ca2+ when cyclic CMP was substrate. Various types of inhibition were observed with different effectors. Cyclic CDP-deoxy cyclic CMP, glutamyl cyclic CMP and 3',5'-cyclic AMP produced competitive inhibition; theophylline produced noncompetitive inhibition; and cytidine 2'-monophosphate 3',5'-cyclic monophosphate, 5-CMP, 2',3'-cyclic CMP, 2',3'-cyclic AMP and 3',5'-cyclic UMP produced mixed type inhibition (either competitive-noncompetitive or uncompetitive-noncompetitive inhibition). Molecular modelling of the substrates and effectors was carried out, and it was deduced that the nitrogen atom bonded to carbon atom 4 (N4) and the oxygen atom bonded to carbon atom 5'(5'-O) with an interatomic distance of 8.92A° was crucial to the binding of ligands; good correlation was obtained between this distance and the potency of the effector. Mass spectrometric analysis suggested that both 5'- and 3'-CMP were products of the enzyme preparation's activity upon 3',5'-cCMP.
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Varandani, Anjali. "Adenosine 3', 5'-cyclic monophosphate activation of islet chloride channels." VCU Scholars Compass, 1998. https://scholarscompass.vcu.edu/etd/5621.

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The objective of this thesis was to understand the regulation of islet Cl⁻ current by cAMP. This current, known as Icl,islet flew is the first Cl⁻ channel current characterized in pancreatic 𝛃 cells. Icl,islet has been hypothesized to modulate insulin secretion through changes in islet electrical activity. Both 5 𝛍M forskolin and 100 𝛍M IBMX (3-isobutyl-1-methylxanthine), agents that increase intracellular cAMP, were shown to activate an outwardly-rectifying ionic current in HIT cells that closely resembled Icl,islet. The current was blocked when iodide was substituted for external Cl⁻ or when the Cl⁻ channel blocker niflumic acid was applied to cells. In contrast, removal of [Na⁺]O did not inhibit the current. In many cells, Cl⁻ current activated and then spontaneously deactivated following cAMP stimulation, suggesting the possibility that the channel desensitizes to [cAMP]i. Exposing cells to multiple cAMP activators revealed that Cl⁻ current declined because it became refractory to increased [cAMP]i. The implication of these results to islet physiology is discussed.
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Hakeem, N.-A. S. "Biochemical studies of cytidine 3', 5'-cyclic monophosphate and other novel endogenous cyclic nucleotides." Thesis, Swansea University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539786.

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Hidir, Saadiah M. "The inhibitory effect of cyclic 3',5' adenosine monophosphate and putrescine in inflammation." Thesis, Aston University, 1985. http://publications.aston.ac.uk/12501/.

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Amini, Fahim. "The role of 3',5'-cyclic adenosine monophosphate (cAMP) in Streptomyces coelicolor A3(2)." Thesis, University of Warwick, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484191.

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Books on the topic "Cyclic guanosine 3',5'-monophosphate"

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Hidir, Saadiah Mohd. The inhibitory effect of cyclic 3',5' adenosine monophosphate and putrescine in inflammation. Birmingham: University of Aston. Department of Pharmacy, 1985.

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Amini, Fahim. The role of 3',5'-cyclic adenosine monophosphate (cAMP) in Streptomyces coelicolor A3(2). 1994.

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Book chapters on the topic "Cyclic guanosine 3',5'-monophosphate"

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Goldberg, Nelson D., and Ann G. O'Toole. "Analysis of Cyclic 3′,5′-Adenosine Monophosphate and Cyclic 3′,5′-Guanosine Monophosphate." In Methods of Biochemical Analysis, 1–39. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/9780470110393.ch1.

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Bartsch, W., K. Strein, E. Böhm, G. Sponer, and B. Müller-Beckmann. "Isosorbide-5-Mononitrate Increases Cyclic Guanosine Monophosphate Concentration in Rat Aorta in Vitro and in Vivo." In Mononitrates, 34–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70234-1_6.

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Lockette, Warren, Yuji Otsuka, and Elizabeth Hirt. "The Endothelium and Cyclic Guanosine Monophosphate in Hyperthyroid-Induced Hypertension." In Vasodepressor Hormones in Hypertension: Prostaglandins and Kallikrein-Kinins, 125–32. Basel: Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9299-5_13.

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Heinemann, L., P. T. Sawicki, G. Stroka, C. Angenvoort, A. Hohmann, and M. Berger. "Cyclic Guanosine Monophosphate Concentrations in Type 1 Diabetic Patients in Different Stages of Diabetic Nephropathy." In Endocrinology of the Heart, 195–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83858-3_34.

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Perez, Dominique, Peter C. Simons, Yelena Smagley, Larry A. Sklar, and Alexandre Chigaev. "A High-Throughput Flow Cytometry Assay for Identification of Inhibitors of 3′,5′-Cyclic Adenosine Monophosphate Efflux." In Methods in Molecular Biology, 227–44. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3673-1_15.

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Sasaki, Fumiaki, Sandra L. Schneider, and Paul M. Zeltzer. "Dibutyryl adenosine 3′:5′-cyclic monophosphate (db-cAMP) induced growth inhibition and morphologic changes in human medulloblastoma cell line TE671." In Biology of Brain Tumour, 27–34. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2297-9_4.

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Scoble, J. E., D. Moskowitz, and K. A. Hruska. "Dibutryladenosine 3’, 5’-Cyclic Monophosphate (dBcAMP) does not Mimic the Action of Parathyroid Hormone (PTH) on Canine Proximal Tubular Basolateral Membrane Na+:Ca2+." In Phosphate and Mineral Homeostasis, 537–41. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_67.

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SAWYER, C., A. HONDA, and W. DOSTMANN. "CygnetsIntracellular Guanosine 3′,5′-Cyclic Monophosphate Sensing in Primary Cells Using Fluorescence Energy Transfer." In Cell Biology, 299–306. Elsevier, 2006. http://dx.doi.org/10.1016/b978-012164730-8/50111-8.

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"Adenosine 3′, 5′ Cyclic Monophosphate (cAMP)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 34. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_264.

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Zakaria, Zainul Amiruddin. "Clinacanthus nutans L., analgesia, and the l-arginine/nitric oxide-mediated/cyclic-guanosine monophosphate-independent pathway." In The Neurobiology, Physiology, and Psychology of Pain, 103–15. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-12-820589-1.00010-5.

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Conference papers on the topic "Cyclic guanosine 3',5'-monophosphate"

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Deweever, A., S. Subedi Paudel, C. Zhou, K. Battle, R. Balczon, D. T. Tambe, and T. Stevens. "Exoenzyme Y - Generated Uridine - 3', 5'- Cyclic Monophosphate Contributes to Pulmonary Edema During Pseudomonas Aeruginosa Infection." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1227.

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Fu, Bingmei M., and Bin Chen. "A Model for the Structural Mechanisms in the Regulation of Microvessel Permeability by cAMP." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/htd-24416.

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Abstract To investigate the microstructural mechanisms of decreasing microvascular permeability induced by the enhancement of intraendothelial adenosine 3’,5’-cyclic monophosphate (cAMP) levels, we extended the previous analytical model developed by Fu et al. (J. Biomech. Eng., 1994) for the interendothelial cleft to include multiple junction strands in the cleft and an interface between the surface glycocalyx layer and the cleft entrance. Based on the electron microscopic observation by Adamson et al. (Am. J. Physiol., 1998), that elevation of intracellular cAMP levels would increase number of tight junction strands, numerical method was applied to test the case in which there are two junction strands in the cleft and there are large discontinuous breaks and a small continuous slit in each strand. Results from this two-junction-strand and two-pore model can successfully account for the experimental data for the decreased permeability to water (Adamson et al. Am. J. Physiol., 1998), small and intermediate-sized solutes (Fu et al., Am. J. Physiol., 1998) by cAMP.
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Pedvis, L. G., T. Wong, J. Wylie, and M. M. Frojmovic. "DIFFERENTIAL INHIBITION OF THE PLATELET ACTIVATION SEQUENCE: SHAPE CHANGE, MICRO- AND MACRO- AGGREGATION, BY A STABLE PROSTACYCLIN ANALOGUE (IL0PR0ST)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643451.

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The relative sensitivities of ADP-induced activation, and prostaglandin-mediated inhibition, were determined for rates of platelet shape change (SC), early platelet recruitment measured by electronic particle counting (PA), and turbidometrically-measured aggregation (TA). Studies were performed in stirred citrated platelet-rich plasma from 7 healthy human donors. The [ADP]½ ([ADP] giving half maximal rate) was determined for the sequence of activation steps expanding on Holmsen’s classical scheme: unactivated platelets → SC → PA → TA. Distinct ADP sensitivities were obtained from log dose-response studies, with a relative dose dependency in the order of [ADP] ½ TA → [ADP] ½ PA → [ADP]> SC of 4:3:1. Sex differences in ADP sensitivities ([ADP]½), for rates of early platelet recruitment measured at 3 seconds were studied from a pool of 20 females and 19 males. Values obtained between the two sexes were comparable (p > 0.05) and independent of hematocrit. Differential inhibition of the above activation scheme was evaluated with Iloprost (ZK 36 374), a stable carbacyclin analogue of prostacyclin (PGI2), with similar potency as PGI2 for the same platelet receptors. Log dose - response curves for inhibition were measured at one high [ADP] (> 1.5 μM) for all 3 parameters, or at respective [ADP]½ values for each parameter. IC5u values ([ZK J causing 50% of inhibition) for inhibition of TA:PA:SC were found in the relative ratios of ∽ 1:3:5, when normalized and expressed as nM ZK per pM ADP used as activator. Thus, ∽ 3x and ∽ 5x more ZK, and likely PGI2, is required to respectively inhibit PA and SC, than that needed to inhibit TA. As observed above for activation, no sex differences in ZK sensitivities were observed (p > 0.1) for 6 males and 6 females. The range of ZK used in this study was below the threshold (∽ 3 nM) generally reported for measurable increases in total basal cyclic 3’ ,5’ adenosine monophosphate (cAMP). This suggests that for each parameter, any increase in cAMP may be associated with selective intracellular pools. The relationship between ZK or PGI2 and intracellular signals remains to be determined.
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