Gotowe bibliografie tematyczne / Adenosine receptors

Gotowa bibliografia na temat „Adenosine receptors”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 11 marca 2023

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Artykuły w czasopismach na temat "Adenosine receptors"

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Dibner-Dunlap, M. E., T. Kinugawa i M. D. Thames. "Activation of cardiac sympathetic afferents: effects of exogenous adenosine and adenosine analogues". American Journal of Physiology-Heart and Circulatory Physiology 265, nr 1 (1.07.1993): H395—H400. http://dx.doi.org/10.1152/ajpheart.1993.265.1.h395.

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Adenosine is released during myocardial ischemia and can cause angina-like chest pain when given by intracoronary administration. We tested the hypothesis that intracoronary adenosine activates cardiac sympathetic afferent fibers and results in reflex sympathoexcitation. In dogs with sinoaortic denervation and vagotomy, we administered 2 mg of adenosine into the left anterior descending artery over 2 min. Before dipyridamole infusion, intracoronary adenosine resulted in no change in blood pressure or renal sympathetic nerve activity. After dipyridamole infusion, which blocks adenosine uptake, intracoronary adenosine resulted in a peak increase in sympathetic activity of 34 +/- 7%. We also investigated the adenosine-receptor subtype responsible for this sympathoexcitatory response. We found that the adenosine1 agonist N6-cyclopentyladenosine elicited a dose-dependent sympathoexcitatory response similar to adenosine but that the adenosine2 agonist 5'-(N-cyclopropyl)carboxamidoadenosine failed to elicit a sympathoexcitatory response. We conclude that adenosine activates cardiac sympathetic afferent fibers and leads to a sympathoexcitatory response due to activation of adenosine1 receptors.
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Vidal, C. "Adenosine and adenosine receptors". Biochimie 74, nr 6 (czerwiec 1992): 591. http://dx.doi.org/10.1016/0300-9084(92)90165-b.

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Steinberg, Thomas H. "Adenosine and Adenosine Receptors". American Journal of Respiratory Cell and Molecular Biology 2, nr 2 (luty 1990): 127–28. http://dx.doi.org/10.1165/ajrcmb/2.2.127.

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Fredholm, Bertil. "Adenosine and adenosine receptors". Trends in Pharmacological Sciences 12 (styczeń 1991): 76. http://dx.doi.org/10.1016/0165-6147(91)90503-k.

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BRUNS, ROBERT F. "Adenosine Receptors." Annals of the New York Academy of Sciences 603, nr 1 Biological Ac (grudzień 1990): 211–25. http://dx.doi.org/10.1111/j.1749-6632.1990.tb37674.x.

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Denton, Kate M. "Adenosine Receptors". Hypertension 72, nr 2 (sierpień 2018): 283–84. http://dx.doi.org/10.1161/hypertensionaha.118.10842.

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Stiles, G. L. "Adenosine receptors." Journal of Biological Chemistry 267, nr 10 (kwiecień 1992): 6451–54. http://dx.doi.org/10.1016/s0021-9258(19)50445-8.

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Ciruela, Francisco. "Adenosine Receptors". Biochimica et Biophysica Acta (BBA) - Biomembranes 1808, nr 5 (maj 2011): 1231–32. http://dx.doi.org/10.1016/j.bbamem.2011.03.007.

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Otah, M. E., i G. L. Stiles. "Adenosine Receptors". Annual Review of Physiology 54, nr 1 (październik 1992): 211–25. http://dx.doi.org/10.1146/annurev.ph.54.030192.001235.

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Palmer, T. M., i G. L. Stiles. "Adenosine receptors". Neuropharmacology 34, nr 7 (lipiec 1995): 683–94. http://dx.doi.org/10.1016/0028-3908(95)00044-7.

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Rozprawy doktorskie na temat "Adenosine receptors"

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Svenningsson, Per. "Striatal adenosine A₂A receptors /". Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19981015sven.

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STEFANELLI, Angela. "Adenosine receptors in health and disease". Doctoral thesis, Università degli studi di Ferrara, 2014. http://hdl.handle.net/11392/2388942.

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Adenosine (Ado) is an endogenous nucleoside released from almost all cell types. It exerts neuroprotective and anti-inflammatory functions by acting through four receptor subtypes A1, A2A, A2B and A3 (ARs). These receptors differ in their affinity for Ado, in the type of G protein that they recruit and finally in the downstream signalling that are activated in target cells. The levels of Ado in the interstitial fluid are in the range of 20-200 nM, but many pathophysiological conditions such as asthma, neurodegenerative disorders, chronic inflammatory diseases and cancer are associated with changes in Ado levels. The primary aim of Ado is to reduce tissue injury and promote repair by different receptor-mediated mechanisms, including the increase of oxygen supply/demand ratio, anti-inflammatory effects and stimulation of angiogenesis. The investigation of ARs and their ligands is a rapidly growing field; there is extensive evidence for the involvement of ARs in the physiological regulation of several homeostatic processes and their implication in the ethiology of many diseases. The aim of this work was to analyse the expression of ARs and the signalling pathway, transcription factors and cytochines activated by them in different pathophysiological conditions linked to hypoxic and inflammatory conditions. At first, the role of ARs was studied in healthy and aneuploid pregnancies to understand reasons of spontaneous abortion (SA). It has been suggested that the causes of SA in aneuploidy are no different to those in euploidy, with the increased frequency in the former perhaps being ascribable to a genetically-determined imbalance in the mediators of placental perfusion and uterine contraction. So aneuploidy can be used as a model of this event. The ado transduction cascade appears to be disturbed in Trisomy 21 (TR21) through reduced expression of A2BAR and A1AR. These anomalies may be implicated in complications such as fetal growth restriction, malformation and/or SA, well known features of aneuploid pregnancies. Therefore A1AR and A2BAR could be potential biomarkers able to provide an early indication of SA risk and their stimulation may turn out to improve fetoplacental perfusion by increasing nitric oxide (NO) and vascular endothelial growth factor (VEGF). Next, the effects of ARs in glial cells under inflammatory conditions have been investigated. Glial cells, astrocytes and microglia, are important contributors to inflammatory immune responses and hypoxia-inducible factor 1 (HIF-1α) is the key transcription factor that is upregulated in response to hypoxia and inflammatory stimuli. Ado, through A1AR and A3AR activation, reduces lipopolysaccharide (LPS)-stimulated HIF-1α mRNA expression and protein accumulation by inhibiting LPS-triggered p42/p44 mitogen-activated protein kinase (p44/42 MAPK) and serine/threonine protein kinase (Akt) phosphorylation in normoxic and hypoxic conditions. This leads to an inhibition of genes involved in inflammation like Inducible Nitric Oxide Synthase (iNOS) and A2BARs, that are stimulated by LPS and further increased by LPS in concert with hypoxia, whilst does not affect angiogenesis and metabolic related genes, with the exception of glucose transporter 1 (GLUT1) and hexokinase 2 (HK2) that are stimulated by LPS in normoxia and reduced by A1AR and A3AR activation. These findings add a new molecular pathway activated by Ado in astrocytes to give a reduction of genes involved in inflammation and hypoxic injury that may cohexist in stroke, ischemia and other central nervous system (CNS) disorders.
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Wang, Jianjie. "Modulation of coronary and skeletal muscle exchange by adenosine : role of adenosine receptors /". Free to MU Campus, others may purchase, 2005. http://wwwlib.umi.com/cr/mo/fullcit?p3204635.

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Cohen, Fiona Rachel. "The allosteric regulation of adenosine receptors". Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309286.

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Scammells, Peter J., i n/a. "Pyrazolo(3,4-d)Pyrimidines and adenosine receptors: a structure/activity study". Griffith University. Division of Science and Technology, 1990. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20050826.141630.

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Pyrazolopyrimidines are a general class of compounds which exhibit Aj adenosine receptor affmity. A number of pyrazolo(3,4-d)pyrimidine analogues of isoguanosine and i-methylisoguanosine has been synthesised. All compounds were tested forAi adenosine receptor affinity using a (311) R-PIA competitive binding assay. The N-i and N-5 positions were substituted with a number of different ailcyl and aryi groups. 3-Chiorophenyl substitution of the N-i position and butyl substitution of the N-5 position greatly enhanced the overall adenosine receptor affinity. Substitution by a methyl group at the N-7 position fixed the C-4 position in the imino tautomeric form. This resulted in a marked reduction in activity. The substitution of the N-2 position with a phenyl group produced an analogue with a similar structure to i,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine (PACPX). A 2-phenyl substituent was favourable for interaction with the adenosine receptor. A number of pyrazolo(3,4-d)pyrirnidine analogues of 4,6-bis-a-carbamoylethylthio-i-phenylthiopyrazolo(3,4-d)pyrinhidine (DJB-KK) has also been synthesised and tested for Aj adenosine receptor affinity. 4,6-Bis-alkylthio-1-phenylpyrazolo(3,4-d)pyrimidines with a-carbamoylethyl and u-carbamoylpropyi groups were compared. The additional methyiene of the a-carbamoylpropyl group produced increased adenosine receptor affinity. 6-a-Carbamoylethylthio-4-mercapto-1-phenylpyrazolo(3,4-d)pyrimidine and 4-cc-carbamoylethylthio- i-phenylpyrazolo(3,4-dlpyrimidine were compared. Substitution of the C-6 position maintained activity, while substitution of the C-4 reduced activity.
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Scammells, Peter. "Pyrazolo(3,4-d)Pyrimidines and adenosine receptors: a structure/activity study". Thesis, Griffith University, 1990. http://hdl.handle.net/10072/365214.

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Pyrazolopyrimidines are a general class of compounds which exhibit Aj adenosine receptor affmity. A number of pyrazolo(3,4-d)pyrimidine analogues of isoguanosine and i-methylisoguanosine has been synthesised. All compounds were tested forAi adenosine receptor affinity using a (311) R-PIA competitive binding assay. The N-i and N-5 positions were substituted with a number of different ailcyl and aryi groups. 3-Chiorophenyl substitution of the N-i position and butyl substitution of the N-5 position greatly enhanced the overall adenosine receptor affinity. Substitution by a methyl group at the N-7 position fixed the C-4 position in the imino tautomeric form. This resulted in a marked reduction in activity. The substitution of the N-2 position with a phenyl group produced an analogue with a similar structure to i,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine (PACPX). A 2-phenyl substituent was favourable for interaction with the adenosine receptor. A number of pyrazolo(3,4-d)pyrirnidine analogues of 4,6-bis-a-carbamoylethylthio-i-phenylthiopyrazolo(3,4-d)pyrinhidine (DJB-KK) has also been synthesised and tested for Aj adenosine receptor affinity. 4,6-Bis-alkylthio-1-phenylpyrazolo(3,4-d)pyrimidines with a-carbamoylethyl and u-carbamoylpropyi groups were compared. The additional methyiene of the a-carbamoylpropyl group produced increased adenosine receptor affinity. 6-a-Carbamoylethylthio-4-mercapto-1-phenylpyrazolo(3,4-d)pyrimidine and 4-cc-carbamoylethylthio- i-phenylpyrazolo(3,4-dlpyrimidine were compared. Substitution of the C-6 position maintained activity, while substitution of the C-4 reduced activity.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Division of Science and Technology
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Hussey, Martin John. "Adenosine Aâ‚‚A receptors and peripheral nociception". Thesis, University of Surrey, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441903.

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Gurden, Mark Francis. "Studies on the classification of adenosine receptors". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386645.

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Torvinen, Maria. "Adenosine receptor/dopamine receptor interactions : molecular and biochemical aspects /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-298-1/.

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Carlos, Carolina Dias. "Polimorfismos nos Receptores de Adenosina, suas Associações com Características Fisiopatológicas e Avaliação de Componentes na Biossíntese da Adenosina em Pacientes com Doença Falciforme". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-12062013-074600/.

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Na Anemia Falciforme em situações de baixa tensão de oxigênio, a hemoglobina mutante S (HbS) sofre polimerização promovendo a falcização das hemácias, que podem aderir ao endotélio vascular, causando a oclusão de vasos (VO) e isquemia tecidual (crises dolorosas) que caracterizam o quadro clínico da doença. Além disso, os pacientes falciformes apresentam outras manifestações clínicas como o priapismo, alterações ósseas, certas complicações pulmonares entre outros. Além das células eritróides, células endoteliais, leucócitos e plaquetas também desempenham um papel fundamental na fisiopatologia da anemia falciforme. A hidroxiuréia (HU), na anemia falciforme, aumenta a produção de hemoglobina fetal (HbF) em células eritróides, reduzindo a polimerização da HbS, diminuindo os sintomas clínicos dos pacientes. O aumento da HbF, no entanto, não implica necessariamente na melhora clínica, indicando desta forma a potencial ação da HU sobre outros processos. Estudos recentes vêm relacionando priapismo e asma com elevados níveis de adenosina. Devido a esta importância da adenosina relacionada a patologias comuns a AF, tivemos como objetivo identificar polimorfismos em genes de receptores de adenosina e na adenosina deaminase e verificar a possível associação entre as manifestações clínicas, além de investigar o papel da HU na modulação de marcadores envolvido na síntese e degradação da adenosina. Foram analisados diversos sítios polimórficos nos genes que codificam ADORA1, ADORA 2b, ADORA 3 e ADA, seguindo com a genotipagem em pacientes com AF, comparando afetados e não afetados. Em adição foi avaliada a expressão diferencial de mRNA de ADA pela HU em monócitos destes pacientes, comparando tratados e não tratados e também avaliamos por citometria de fluxo a modulação de marcadores de superfície CD39, CD73 e CD26, pela HU. As análises estatísticas foram realizadas utilizando os softwares GenePop 3.4 para análises de associação, cálculo do HWE, GraphPad Prism 5, Arlequin para identificação de desequilíbrio de ligação, haplótipos, heterozigozidade e SAS 9.13 para associação dos haplótipos as características. Os resultados mostraram que os pacientes sob tratamento com HU apresentaram um aumento da expressão de mRNA de ADA, aumento da expressão de CD26 em monócitos e diminuição de CD39 em linfócitos. Sem alterações significativas em relação a CD73. Encontramos também um aumento da freqüência do alelo T do SNP (rs1685103) presente no gene de ADORA 1 associado com pacientes afetados com síndrome torácica aguda. Apesar de não ter sido estatisticamente significante, concorda com dados da literatura. No gene ADORA 2B, verificamos associação do SNP 1007 C>T no desenvolvimento de STA indicando o alelo T como fator de risco e o alelo C para alterações ósseas. Para o SNP 968 G>T houve associação com alterações ósseas. Na análise haplotípica entre os SNPs 968 G>T e 1007 C>T encontramos associação dos haplótipos ht2 e ht3 com STA, como fator de risco, ht2 para hipertensão pulmonar. ht1 para priapismo, alterações ósseas e estenose/AVC. Os haplótipos formados pelos três SNPs 968 G>T, 1007 C>T e rs16851030, encontramos associação entre ht1, ht3 e ht4 entre os afetados com priapismo, caracterizando-o como haplótipo de risco e também ht1 e ht6 associados à estenose/AVC. Concluímos, que a hidroxiuréia participa na modulação da expressão da adenosina deaminase, de CD26 em monócitos e CD39 em linfócitos. Além disso, mostrou-se a importância de sítios polimórfico presente no gene ADORA 2B e ADORA1 envolvido na fisiopatologia das manifestações clínicas da doença falciforme. Associações dos SNPs em ADORA 1 e ADA, devem ser melhor estudados em um número maior de pacientes. A determinação destes polimorfismos associados com diferentes características clínicas pode levar a um melhor entendimento dos processos fisiopatológicos da anemia falciforme, levando à identificação de pacientes de risco, possibilitando um manejamento racional dos mesmos, em termos de cuidados específicos, ou mesmo à determinação de alvos para o desenvolvimento de terapias alternativas.
In sickle cell disease in low oxygen tension, mutant hemoglobin S (HbS) undergoes polymerization promoting sickling of red blood cells that can adhere to vascular endothelium, causing vessel occlusion (VO) and tissue ischemia (painful crises) that characterize the clinical disease. In addition, sickle cell patients have other clinical manifestations such as priapism, bone disorders, certain pulmonary complications among others. In addition to the erythroid cells, endothelial cells, white cells and platelets also play a key role in the pathophysiology of sickle cell anemia. Hydroxyurea (HU) in sickle cell anemia, increases the production of fetal hemoglobin (HbF) in erythroid cells, reducing the HbS polymerization, reducing the clinical symptoms of patients. The increase in HbF, however, does not necessarily imply clinical improvement, thus indicating the potential effects of HU on other processes. Recent studies relating asthma and priapism with high levels of adenosine. Due to this importance of adenosine-related pathologies common to AF, we aimed to identify gene polymorphisms in adenosine receptors and adenosine deaminase and verify the possible association between clinical manifestations, and to investigate the role of HU in the modulation of markers involved synthesis and degradation of adenosine. We analyzed several polymorphic sites in genes that encode ADORA1, ADORA 2b, 3 and ADORA ADA, according to the genotype in patients with AF, comparing affected and unaffected. In addition we assessed the differential expression of ADA mRNA by HU in monocytes of these patients, comparing treated and untreated, and also evaluated by flow cytometry modulation of surface markers CD39, CD73 and CD26 by HU. Statistical analysis was performed using the software GenePop 3.4 for association analysis, calculation of HWE, GraphPad Prism 5, Arlequin for identification of linkage disequilibrium, haplotypes, heterozygosity and SAS 9.13 for association of haplotypes features. The results showed that patients treated with HU showed an increase in mRNA expression of ADA, increased expression of CD26 on monocytes and decreased CD39 on lymphocytes. No significant changes in relation to CD73. We also found an increased frequency of allele T (SNP rs1685103) present in a gene associated with ADORA affected patients with acute chest syndrome. Although not statistically significant, agrees with literature data. ADORA 2B gene, we found association of the SNP 1007 C> T in the development of STA indicating the T allele as a risk factor for the C allele and bone changes. For the SNP 968 G> T was associated with bone disorders. In haplotype analysis between SNPs 968 G> T and 1007 C> T found association of haplotypes ht2 and HT3 with STA as a risk factor for pulmonary hypertension ht2. ht1 for priapism, stenosis and bone disorders / stroke. The three haplotypes formed by SNPs 968 G> T, 1007 C> T and rs16851030, we found association between ht1, HT3 and HT4 among those affected with priapism, characterizing it as a risk haplotype and also ht1 ht6 associated with renal and / AVC. We conclude that hydroxyurea participates in modulating the expression of adenosine deaminase of CD26 on monocytes and CD39 on lymphocytes. Moreover, he showed the importance of polymorphic sites in this gene and ADORA 2B ADORA1 involved in the pathophysiology of clinical manifestations of sickle cell disease. Associations of SNPs in ADORA 1 and ADA should be better studied in a larger number of patients. The determination of these polymorphisms associated with different clinical characteristics can lead to a better understanding of the pathophysiological processes of sickle cell anemia, leading to the identification of patients at risk, enabling a rational handling of the same in terms of specific care, or even the determination of targets for the development of alternative therapies.
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Książki na temat "Adenosine receptors"

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Williams, Michael, red. Adenosine and Adenosine Receptors. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9.

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Williams, Michael, 1947 Jan. 3-, red. Adenosine and adenosine receptors. Clifton, N.J: Humana Press, 1990.

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F, Cooper Dermot M., i Londos Constantine, red. Adenosine receptors. New York: A.R. Liss, 1988.

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Borea, Pier Andrea, Katia Varani, Stefania Gessi, Stefania Merighi i Fabrizio Vincenzi, red. The Adenosine Receptors. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90808-3.

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Hiroshi, Kase, Richardson Peter J i Jenner P. G, red. Adenosine receptors and Parkinson's disease. San Diego, Calif: Academic, 2000.

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Hiroshi, Kase, Richardson Peter J i Jenner Peter 1946-, red. Adenosine receptors and Parkinson's disease. San Diego, CA: Academic Press, 2000.

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Wilson, Constance N., i S. Jamal Mustafa, red. Adenosine Receptors in Health and Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89615-9.

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A, Ribeiro J., red. Adenosine receptors in the nervous system. London: Taylor & Francis, 1989.

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service), SpringerLink (Online, red. Adenosine receptors in health and disease. Dordrecht: Springer, 2009.

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A3 adenosine receptors from cell biology to pharmacology and therapeutics. Dordrecht: Springer, 2010.

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Części książek na temat "Adenosine receptors"

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Williams, Michael. "Adenosine Receptors". W Adenosine and Adenosine Receptors, 1–15. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_1.

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Williams, Michael. "Adenosine Receptors". W Adenosine and Adenosine Receptors, 501–7. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_13.

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Griffiths, Timothy L., i Stephen T. Holgate. "The Role of Adenosine in Respiratory Physiology". W Adenosine and Adenosine Receptors, 381–422. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_10.

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Jarvis, Michael F., i Michael Williams. "Adenosine in Central Nervous System Function". W Adenosine and Adenosine Receptors, 423–74. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_11.

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Cronstein, Bruce N., i Rochelle Hirschhorn. "Adenosine and Host Defense". W Adenosine and Adenosine Receptors, 475–500. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_12.

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Williams, Michael, i Kenneth A. Jacobson. "Radioligand Binding Assays for Adenosine Receptors". W Adenosine and Adenosine Receptors, 17–55. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_2.

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Trivedi, Bharat K., Alexander J. Bridges i Robert F. Bruns. "Structure-Activity Relationships of Adenosine A1 and A2 Receptors". W Adenosine and Adenosine Receptors, 57–103. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_3.

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Cooper, Dermot M. F., i Kevin K. Caldwell. "Signal Transduction Mechanisms for Adenosine". W Adenosine and Adenosine Receptors, 105–41. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_4.

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Dunwiddie, Thomas V. "Electrophysiological Aspects of Adenosine Receptor Function". W Adenosine and Adenosine Receptors, 143–72. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_5.

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Stone, Trevor W., Andrew C. Newby i Hilary G. E. Lloyd. "Adenosine Release". W Adenosine and Adenosine Receptors, 173–223. Totowa, NJ: Humana Press, 1990. http://dx.doi.org/10.1007/978-1-4612-4504-9_6.

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Streszczenia konferencji na temat "Adenosine receptors"

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Lin, Juqiang, Yating Lin, Yiming Huang, Zhiwei Wu, Jianshu Xu, Ya Hu i Shusen Xie. "Quantitative FRET measurement of the interaction of A1 adenosine receptors and A2A adenosine receptors in living cell". W Optics in Health Care and Biomedical Optics VIII, redaktorzy Qingming Luo, Xingde Li, Yuguo Tang i Ying Gu. SPIE, 2018. http://dx.doi.org/10.1117/12.2500692.

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Bowry, S. K., i M. Tepel. "NON-REVERSIBLE BINDING OF 5'-p-FLUOROSULFONYLBENZOYL ADENOSINE TO WASHED INTACT PLATELETS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643506.

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ADP is an important in vivo mediator of platelet aggregation. The identification and estimation of a finite number of receptor sites has been made difficult by the reversible nature of the action of ADP on platelets and because ADP can be degraded by enzymes on the platelet surface. Analogues of ADP have therefore been commonly used to study the ADP receptor. We investigated the validity of using 5'-p-fluorosulfonylbenzoyl adenosine (FSBA), an affinity analogue of ADP that inhibits ADP-induced aggregation, for studying the ADP receptor on intact washed platelets. Binding of labelled FSBA, like for ADP, was saturable. Scatchard plot analyses of equilibrium binding data indicated, positive cooperativity; the apparent affinity (2.4 × 10−6) correlated well with the amount of ADP required to cause aggregation and with the value obtained from aggregation studies. However, the platelet bound FSBA was not displaceable with excess unlabelled FSBA indicating non-reversibility of ligand binding. As the minimal criteria for receptor identification (specificity, saturability and reversibility) are not fulfilled, the usage of FSBA to study the ADP receptor must be treated with caution. As FSBA is able to bind covalently to at least four polypeptides in isolated platelet membranes, a finite number of receptors cannot be postulated using FSBA. Furthermore, positive cooperativity, as indicated by the Scatchard plots, may be explained in terms of specific non-receptor binding. As the ADP receptor cannot be identified with any degree of certainty, the possibility therfore exists that the mechanism by which ADP initiates aggregation by rearrangement of platelet membrane proteins without binding to a single protein receptor.
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Maciaszek, J. L., B. Andemariam i G. Lykotrafitis. "Red Blood Cell Surface Receptor Expression of BCAM/Lu is Regulated by Protein Kinase A Activity". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14311.

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Irregular sickle red blood cells (RBCs) can contribute to the pathogenesis of vasoocclusion and other complications of sickle cell disease (SCD) via abnormal adherence to the vascular endothelium. It has previously been demonstrated that epinephrine enhances SCD RBC adhesion by activating the BCAM/Lu and ICAM-4 surface receptors [1–2]. Epinephrine acts on the RBC β2-adrenergic receptor, thereby activating Gas proteins that stimulate adenylyl cyclase (AC). This enzyme catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), leading to protein kinase A (PKA) activation, an intermediate step in the upregulation of BCAM/Lu and ICAM-4 mediated adhesion. The interaction of BCAM/Lu with the α5 chain of laminin may contribute to vaso-occlusive events in SCD due to overexpression of BCAM on SCD RBCs.
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CUNHA, R. A. "SCNS.01. Adenosine receptors and brain diseases: neuroprotection and neurodegeneration". W I International Symposium in Neuroscience Meeting. Editora Edgard Blücher, 2014. http://dx.doi.org/10.5151/isnm-sine2.

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DiRenzo, Daniel, Dana Piovesan, Joanne Tan, Dillon H. Miles, Manmohan R. Leleti, Timothy Park, Ferdie Soriano i in. "Abstract A162: AB928, a dual antagonist of the A2aR and A2bR adenosine receptors, relieves adenosine-mediated immune suppression". W Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a162.

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Volpini, Rosaria, Catia Lambertucci, Sara Taffi, Sauro Vittori, Karl-Norbert Klotz i Gloria Cristalli. "A3 adenosine receptors: Synthesis and biological evaluation of new potent and selective ligands". W XIIIth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2005. http://dx.doi.org/10.1135/css200507297.

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Umapathy, Nagavedi S., Elzbieta Kaczmarek, Rudolf Lucas, Kurt Stenmark, Alexander D. Verin i Evgenia Gerasimovskaya. "Adenosine A1 Receptors Mediated Enhancement Of Barrier Function In Vasa Vasorum Endothelial Cells". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1872.

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Huang, Yimei, Hongqin Yang, Liqin Zheng, Jiangxu Chen, Yuhua Wang, Hui Li i Shusen Xie. "Investigating real-time activation of adenosine receptors by bioluminescence resonance energy transfer technique". W SPIE BiOS, redaktorzy Samuel Achilefu i Ramesh Raghavachari. SPIE, 2013. http://dx.doi.org/10.1117/12.2005507.

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Lin, Yating, Jianshu Xu, Jiamin Gao, Yimei Huang, Qiwen Wang, Shusen Xie i Juqiang Lin. "Real-time calcium imaging by the interaction of adenosine receptors in living HEK293T cells". W Optics in Health Care and Biomedical Optics X, redaktorzy Qingming Luo, Xingde Li, Ying Gu i Dan Zhu. SPIE, 2020. http://dx.doi.org/10.1117/12.2573547.

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Agarwal, Kailash C. "NEW INSIGHTS INTO THE ANTIPLATELET ACTIVITY OF FORSKOLIN: ROLE OF PLASMA ADENOSINE AND SPECIES DIFFERENCES". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643584.

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Forskolin stimulates adenylate cyclase by interacting with the catalytic subunit and inhibits platelet aggregation. This inhibition is greatly potentiated by adenosine (Ado) which stimulates adenylate cyclase through membrane-bound Ado receptors. Forskolin is 2-4 fold more potent as an inhibitor of collagen-induced rat platelet aggregation as compared to human platelets (IC50 values, in rat PRP, 0.5-0.8 μM; in human PRP, 1.5-2 μM). However, if the blood is pretreated with adenosine deaminase (ADA), an enzyme that degrades Ado to inosine, the inhibitory action of forskolin is greatly reduced producing similar effects both in human and rat PRPs (IC50, 2-3 μM) and whole blood (IC50, 4.6 μM). Both 5’-methylthioadenosine (MTA, 50-100 μM), an antagonist of Ado receptors, and 2’,5’-dideoxyadenosine (DDA, 100 μM), an inhibitor of adenylate cyclase, reverse the inhibition of platelet aggregation in rat PRP, whereas, no reversal is seen in human PRP. When Ado in the rat plasma is degraded by ADA pretreatment, DDA or MTA shows no reversal as seen in human PRP. The inhibitory action of forskolin (1-2 μM), which is only weakly inhibitory alone (<20%) in human whole blood, can be greatly potentiated (100% inhibition) by the inhibitors of nucleoside transport, dipyridamole (10 μM) or dilazep (2 μM). Only slight potentiation is seen in rat whole blood suggesting that rat plasma Ado levels are not affected significantly perhaps due to weakly active erythrocytic nucleoside transport system. Sato and Ui (In: Physiology and Pharmacology of Adenosine, Daly et al, Eds. Raven Press, 1983, 1-11), have shown that rat plasma contains much higher Ado levels (7.55 ± 0.51 pM) than human plasma (0.29 ± 0.08 μM). These studies demonstrate that plasma adenosine plays an important role in the forskolin antiplatelet activity which can be greatly potentiated in human whole blood by the clinically used drugs, dipyridamole and dilazep. (Supported by US PHS Grant CA 07340).
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Raporty organizacyjne na temat "Adenosine receptors"

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Schwarzshild, Michael A. Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, październik 2006. http://dx.doi.org/10.21236/ada462198.

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Schwarzschild, Michael A. Caffeine, Adenosine Receptors and Estrogen in Toxin Models of Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, październik 2009. http://dx.doi.org/10.21236/ada625341.

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Liou, Gregory I., Saif Ahmad, Mohammad Naime, Nadeem Fatteh i Sohail Khan. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2012. http://dx.doi.org/10.21236/ada581642.

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Liou, Gregory I., Saif Ahmad i Ahmed Elsherbini. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2013. http://dx.doi.org/10.21236/ada600384.

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Ye, Libin, Christopher Andrew Neale, Adnan Sljoka, Brent Lyda, Dmitry Pichugin, Nobuyuki Tsuchimura, Sacha T. Larda i in. Mechanistic insights into allosteric regulation of the A2A adenosine G protein-coupled receptor by physiological cations. Office of Scientific and Technical Information (OSTI), kwiecień 2018. http://dx.doi.org/10.2172/1434450.

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