Relevant bibliographies by topics / Adenosine A2B receptor

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Academic literature on the topic 'Adenosine A2B receptor'

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Published: 10 March 2023

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Journal articles on the topic "Adenosine A2B receptor"

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Wolska, Nina, and Marcin Rozalski. "Blood Platelet Adenosine Receptors as Potential Targets for Anti-Platelet Therapy." International Journal of Molecular Sciences 20, no. 21 (November 3, 2019): 5475. http://dx.doi.org/10.3390/ijms20215475.

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Adenosine receptors are a subfamily of highly-conserved G-protein coupled receptors. They are found in the membranes of various human cells and play many physiological functions. Blood platelets express two (A2A and A2B) of the four known adenosine receptor subtypes (A1, A2A, A2B, and A3). Agonization of these receptors results in an enhanced intracellular cAMP and the inhibition of platelet activation and aggregation. Therefore, adenosine receptors A2A and A2B could be targets for anti-platelet therapy, especially under circumstances when classic therapy based on antagonizing the purinergic receptor P2Y12 is insufficient or problematic. Apart from adenosine, there is a group of synthetic, selective, longer-lasting agonists of A2A and A2B receptors reported in the literature. This group includes agonists with good selectivity for A2A or A2B receptors, as well as non-selective compounds that activate more than one type of adenosine receptor. Chemically, most A2A and A2B adenosine receptor agonists are adenosine analogues, with either adenine or ribose substituted by single or multiple foreign substituents. However, a group of non-adenosine derivative agonists has also been described. This review aims to systematically describe known agonists of A2A and A2B receptors and review the available literature data on their effects on platelet function.
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Feng, Ming-Guo, and L. Gabriel Navar. "Afferent arteriolar vasodilator effect of adenosine predominantly involves adenosine A2B receptor activation." American Journal of Physiology-Renal Physiology 299, no. 2 (August 2010): F310—F315. http://dx.doi.org/10.1152/ajprenal.00149.2010.

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Adenosine is an important paracrine agent regulating renal vascular tone via adenosine A1 and A2 receptors. While A2B receptor message and protein have been localized to preglomerular vessels, functional evidence on the role of A2B receptors in mediating the vasodilator action of adenosine on afferent arterioles is not available. The present study determined the role of A2B receptors in mediating the afferent arteriolar dilation and compared the effects of A2B and A2A receptor blockade on afferent arterioles. We used the rat in vitro blood-perfused juxtamedullary nephron technique combined with videomicroscopy. Single afferent arterioles of Sprague-Dawley rats were visualized and superfused with solutions containing adenosine or adenosine A2 receptor agonist (CV-1808) along with adenosine A2B and A2A receptor blockers. Adenosine (10 μmol/l) caused modest constriction and subsequent superfusion with SCH-58261 (SCH), an A2A receptor blocker, at concentrations up 10 μmol/l elicited only slight additional decreases in afferent arteriolar diameter with maximum effect at a concentration of 1 μmol/l (−11.0 ± 2.5%, n = 6, P < 0.05). However, superfusion of adenosine-treated vessels with MRS-1754 (MRS), an A2B receptor blocker, elicited greater decreases in afferent arteriolar diameter (−26.0 ± 4.7%, n = 5, P < 0.01). SCH did not significantly augment the adenosine-mediated afferent constriction elicited by MRS; however, adding MRS after SCH caused further significant vasoconstriction. Superfusion with CV-1808 dilated afferent arterioles (17.2 ± 2.4%, n = 6, P < 0.01). This effect was markedly attenuated by MRS (−22.6 ± 2.0%, n = 5, P < 0.01) but only slightly reduced by SCH (−9.0 ± 1.1%, n = 5, P < 0.05) and completely prevented by adding MRS after SCH (−24.7 ± 1.8%, n = 5, P < 0.01). These results indicate that, while both A2A and A2B receptors are functionally expressed in juxtamedullary afferent arterioles, the powerful vasodilating action of adenosine predominantly involves A2B receptor activation, which counteracts A1 receptor-mediated vasoconstriction.
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Gebremedhin, Debebe, Brian Weinberger, David Lourim, and David R. Harder. "Adenosine Can Mediate its Actions through Generation of Reactive Oxygen Species." Journal of Cerebral Blood Flow & Metabolism 30, no. 10 (June 9, 2010): 1777–90. http://dx.doi.org/10.1038/jcbfm.2010.70.

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Adenosine is an important cerebral vasodilator, but mediating mechanisms are not understood. We investigated the expression of adenosine receptor subtypes in isolated cerebral arterial muscle cells (CAMCs), and their role in adenosine-induced superoxide (O2−) generation and reduction in cerebral arterial tone. Reverse transcriptase-PCR, western blotting, and immunofluorescence studies have shown that CAMCs express transcript and protein for A1, A2A, A2B, and A3 adenosine receptors. Stimulation of CAMCs with adenosine or the A2A agonist CGS-21680 increased the generation of O2− that was attenuated by the inhibition of A2A and A2B adenosine receptor subtypes, or by the peptide inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase gp91ds-tat, or by the mitochondria uncoupler 2,4-dinitrophenol. Application of adenosine or CGS-21680 dilated pressure-constricted cerebral arterial segments that were prevented by the antioxidants superoxide dismutase (SOD) conjugated to polyethylene glycol (PEG) and PEG-catalase or by the A2B adenosine receptor antagonist MRS-1754, or by the mixed A2A and A2B antagonist ZM-241385. Antagonism of the A2A and A2B adenosine receptors had no effect on cerebral vasodilatation induced by nifedipine. These findings indicate that adenosine reduces pressure-induced cerebral arterial tone through stimulation of A2A and A2B adenosine receptors and generation of O2− from NADPH oxidase and mitochondrial sources. This signaling pathway could be one of the mediators of the cerebral vasodilatory actions of adenosine.
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Zaynagetdinov, Rinat, Kai Schiemann, Kalyan Nallaparaju, Natalya Belousova, Armine Matevossian, Zhouxiang Chen, Giorgio Kradjian, et al. "Abstract 3499: M1069 as dual A2A/A2B adenosine receptor antagonist counteracts immune-suppressive mechanisms of adenosine and reduces tumor growth in vivo." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3499. http://dx.doi.org/10.1158/1538-7445.am2022-3499.

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Abstract Under physiological conditions, the extracellular concentrations of adenosine are low, however, levels dramatically increase under metabolically stressful conditions, including inflammation and cancer. The regulatory functions of adenosine are mediated through four members of the adenosine receptor family: A1, A2A, A2B, and A3. While A2A was considered the major contributor to adenosine-mediated suppression of T cell, natural killer cell, and myeloid cell functions, A2B has also recently emerged as a potential modulator of these processes. Both A2A and A2B signal through the same Gs-mediated activation of adenylate cyclase, which can allow the lower affinity A2B receptor to compensate for the inhibition of A2A in an adenosine-rich tumor microenvironment (TME). A2B receptors are also reported to support tumor growth independent of A2A through the Gq subunit of G-protein-coupled receptor-mediated production of vascular endothelial growth factor (VEGF) by myeloid and tumor cells. Therefore, simultaneous targeting of both the A2A and A2B receptors may provide a higher potential for cancer immunotherapy in an adenosine-rich TME, where A2B can act in compensatory or complementary means to A2A. M1069 is a small-molecule, dual antagonist of the A2A and A2B adenosine receptors with a selectivity of &gt;100 fold against the A1 and A3 receptors. In assays with primary human T cells, M1069 caused a dose-dependent suppression of 5′-N-ethylcarboxamide adenosine (stable analog of adenosine)-stimulated cyclic adenosine monophosphate (cAMP) and phosphorylated cAMP- response element binding protein (pCREB) induction and rescue of interleukin (IL)-2 production (A2A readout). M1069 also suppressed VEGF production from human macrophages (A2B readout) in adenosine-rich settings. M1069 exhibited superior suppression of protumorigenic cytokine secretion, including CXCL1, CXCL5 and granulocyte-colony stimulating factor, and the rescue of IL12 secretion from adenosine-differentiated dendritic cells, as compared to an A2Aselective antagonist. In addition, in a one-way mixed lymphocyte reaction assay, adenosine-differentiated dendritic cells treated with M1069 demonstrated superior T cell activation compared to adenosine-differentiated dendritic cells treated with an A2A-selective antagonist. These findings were further corroborated with the results from in vivo studies in a murine CD73hi/adenosine-rich 4T1 syngeneic breast tumor model, in which M1069, but not an A2A-selective antagonist, reduced tumor growth as a monotherapy and enhanced anti-tumor activity with chemotherapeutic agents. In summary, M1069 is a potent, dual A2A/A2B adenosine receptor antagonist, which is expected to counteract immune-suppressive mechanisms in the presence of high concentrations of adenosine and enhance the anti-tumor activity of chemotherapies. Citation Format: Rinat Zaynagetdinov, Kai Schiemann, Kalyan Nallaparaju, Natalya Belousova, Armine Matevossian, Zhouxiang Chen, Giorgio Kradjian, Meghana Pandya, Nemisha Dawra, Eva-Maria Krauel, Elissaveta Petrova, Oliver Poeschke, David Fischer, Marc Lecomte, Andree Blaukat, Bayard Huck, Jacques Moisan. M1069 as dual A2A/A2B adenosine receptor antagonist counteracts immune-suppressive mechanisms of adenosine and reduces tumor growth in vivo [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3499.
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Xaus, Jordi, Maribel Mirabet, Jorge Lloberas, Concepció Soler, Carme Lluis, Rafael Franco, and Antonio Celada. "IFN-γ Up-Regulates the A2B Adenosine Receptor Expression in Macrophages: A Mechanism of Macrophage Deactivation." Journal of Immunology 162, no. 6 (March 15, 1999): 3607–14. http://dx.doi.org/10.4049/jimmunol.162.6.3607.

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Abstract Adenosine is a potent endogenous anti-inflammatory agent released by cells in metabolically unfavorable conditions, such as hypoxia or ischemia. Adenosine modulates different functional activities in macrophages. Some of these activities are believed to be induced through the uptake of adenosine into the macrophages, while others are due to the interaction with specific cell surface receptors. In murine bone marrow-derived macrophages, the use of different radioligands for adenosine receptors suggests the presence of A2B and A3 adenosine receptor subtypes. The presence of A2B receptors was confirmed by flow cytometry using specific Abs. The A2B receptor is functional in murine macrophages, as indicated by the fact that agonists of A2B receptors, but not agonists for A1, A2A, or A3, lead to an increase in cAMP levels. IFN-γ up-regulates the surface protein and gene expression of the A2B adenosine receptor by induction of de novo synthesis. The up-regulation of A2B receptors correlates with an increase in cAMP production in macrophages treated with adenosine receptor agonist. The stimulation of A2B receptors by adenosine or its analogues inhibits the IFN-γ-induced expression of MHC class II genes and also the IFN-γ-induced expression of nitric oxide synthase and of proinflammatory cytokines. Therefore, the up-regulation of the A2B adenosine receptor expression induced by IFN-γ could be a feedback mechanism for macrophage deactivation.
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Shi, Yanrong, Xiaoguang Liu, Debebe Gebremedhin, John R. Falck, David R. Harder, and Raymond C. Koehler. "Interaction of Mechanisms Involving Epoxyeicosatrienoic Acids, Adenosine Receptors, and Metabotropic Glutamate Receptors in Neurovascular Coupling in Rat Whisker Barrel Cortex." Journal of Cerebral Blood Flow & Metabolism 28, no. 1 (May 23, 2007): 111–25. http://dx.doi.org/10.1038/sj.jcbfm.9600511.

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Adenosine, astrocyte metabotropic glutamate receptors (mGluRs), and epoxyeicosatrienoic acids (EETs) have been implicated in neurovascular coupling. Although A2A and A2B receptors mediate cerebral vasodilation to adenosine, the role of each receptor in the cerebral blood flow (CBF) response to neural activation remains to be fully elucidated. In addition, adenosine can amplify astrocyte calcium, which may increase arachidonic acid metabolites such as EETs. The interaction of these pathways was investigated by determining if combined treatment with antagonists exerted an additive inhibitory effect on the CBF response. During whisker stimulation of anesthetized rats, the increase in cortical CBF was reduced by approximately half after individual administration of A2B, mGluR and EET antagonists and EET synthesis inhibitors. Combining treatment of either a mGluR antagonist, an EET antagonist, or an EET synthesis inhibitor with an A2B receptor antagonist did not produce an additional decrement in the CBF response. Likewise, the CBF response also remained reduced by ∼50% when an EET antagonist was combined with an mGluR antagonist or an mGluR antagonist plus an A2B receptor antagonist. In contrast, A2A and A3 receptor antagonists had no effect on the CBF response to whisker stimulation. We conclude that (1) adenosine A2B receptors, rather than A2A or A3 receptors, play a significant role in coupling cortical CBF to neuronal activity, and (2) the adenosine A2B receptor, mGluR, and EETs signaling pathways are not functionally additive, consistent with the possibility of astrocytic mGluR and adenosine A2B receptor linkage to the synthesis and release of vasodilatory EETs.
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Marquardt, D. L., L. L. Walker, and S. Heinemann. "Cloning of two adenosine receptor subtypes from mouse bone marrow-derived mast cells." Journal of Immunology 152, no. 9 (May 1, 1994): 4508–15. http://dx.doi.org/10.4049/jimmunol.152.9.4508.

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Abstract Adenosine potentiates the stimulated release of mast cell mediators. Pharmacologic studies suggest the presence of two adenosine receptors, one positively coupled to adenylate cyclase and the other coupled to phospholipase C activation. To identify mast cell adenosine receptor subtypes, cDNAs for the A1 and A2a adenosine receptors were obtained by screening a mouse brain cDNA library with the use of PCR-derived probes. Mouse bone marrow-derived mast cell cDNA libraries were constructed and screened with the use of A1 and A2a cDNA probes, which revealed the presence of A2a, but not A1, receptor clones. A putative A2b receptor was identified by using low stringency mast cell library screening. Northern blotting of mast cell poly(A)+ RNA with the use of receptor subtype probes labeled single mRNA bands of 2.4 kb and 1.8 kb for the A2a and A2b receptors, respectively. In situ cells. An A2a receptor-specific agonist failed to enhance mast cell mediator release, which suggests that the secretory process is modulated through the A2b and/or another receptor subtype. By using RNase protection assays, we found that mast cells that had been cultured in the presence of N-ethylcarboxamidoadenosine for 24 h exhibited a decrease in both A2a and A2b receptor RNA levels. Cells that had been cultured for 1 to 2 days in the presence of dexamethasone demonstrated increased amounts of A2a receptor mRNA, but no identifiable change in A2b receptor mRNA. Mast cells possess at least two adenosine receptor subtypes that may be differentially regulated.
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Dubey, Raghvendra K., Delbert G. Gillespie, and Edwin K. Jackson. "A2B Adenosine Receptors Mediate the Anti-Mitogenic Effects of Adenosine in Cardiac Fibroblasts." Hypertension 36, suppl_1 (October 2000): 708. http://dx.doi.org/10.1161/hyp.36.suppl_1.708-b.

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P85 Adenosine inhibits growth of CFs; however, the adenosine receptor subtype that mediates this anti-mitogenic effect remains undefined. Using specific ADE receptor antagonists and agonists and antisense oligonucleotides (OLIGO) against A2B receptors, we investigated the role of A2B receptors in inhibiting cardiac fibroblast growth. PDGF (25ng/ml)-induced DNA synthesis, cell number and collagen synthesis in CFs were inhibited by A2 (chloroadenosine [Cl-Ad]and MECA), but not by A1 (CPA), A2a ( CGS21680 ) or A3 (AB-MECA),receptor agonists.The inhibitory effects of 1μM MECA and Cl-Ad were reversed by A1/A2 (DPSPX; 10nM), but not by A1 (DPCPX; 10nM), receptor antagonists. In CFs treated with antisense, but not sense or scrambled, OLIGOs to the A2B receptor, both basal and PDGF-induced DNA synthesis was enhanced by 70±4% and 64±5% respectively. Moreover, the inhibitory effects of Cl-Ad and MECA were completely abolished in CFs treated with antisense, but not sense and scrambled, OLIGOs. In conclusion, A2B receptors mediate the anti-mitogenic effects of adenosine suggesting that A2B receptors are importantly involved in the regulation of CF biology. Thus, A2B receptors may play a critical role in regulating cardiac remodeling associated with CF proliferation.
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Zhan, Enbo, Victoria J. McIntosh, and Robert D. Lasley. "Adenosine A2A and A2B receptors are both required for adenosine A1 receptor-mediated cardioprotection." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (September 2011): H1183—H1189. http://dx.doi.org/10.1152/ajpheart.00264.2011.

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All four adenosine receptor subtypes have been shown to play a role in cardioprotection, and there is evidence that all four subtypes may be expressed in cardiomyocytes. There is also increasing evidence that optimal adenosine cardioprotection requires the activation of more than one receptor subtype. The purpose of this study was to determine whether adenosine A2A and/or A2B receptors modulate adenosine A1 receptor-mediated cardioprotection. Isolated perfused hearts of wild-type (WT), A2A knockout (KO), and A2BKO mice, perfused at constant pressure and constant heart rate, underwent 30 min of global ischemia and 60 min of reperfusion. The adenosine A1 receptor agonist N6-cyclohexyladenosine (CHA; 200 nM) was administrated 10 min before ischemia and for the first 10 min of reperfusion. Treatment with CHA significantly improved postischemic left ventricular developed pressure (74 ± 4% vs. 44 ± 4% of preischemic left ventricular developed pressure at 60 min of reperfusion) and reduced infarct size (30 ± 2% with CHA vs. 52 ± 5% in control) in WT hearts, effects that were blocked by the A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (100 nM). Treatments with the A2A receptor agonist CGS-21680 (200 nM) and the A2B agonist BAY 60-6583 (200 nM) did not exert any beneficial effects. Deletion of adenosine A2A or A2B receptor subtypes did not alter ischemia-reperfusion injury, but CHA failed to exert a cardioprotective effect in hearts of mice from either KO group. These findings indicate that both adenosine A2A and A2B receptors are required for adenosine A1 receptor-mediated cardioprotection, implicating a role for interactions among receptor subtypes.
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Lu, Qing, Elizabeth O. Harrington, Julie Newton, Brian Casserly, Gregory Radin, Rod Warburton, Yang Zhou, Michael R. Blackburn, and Sharon Rounds. "Adenosine protected against pulmonary edema through transporter- and receptor A2-mediated endothelial barrier enhancement." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 6 (June 2010): L755—L767. http://dx.doi.org/10.1152/ajplung.00330.2009.

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We have previously demonstrated that adenosine plus homocysteine enhanced endothelial basal barrier function and protected against agonist-induced barrier dysfunction in vitro through attenuation of RhoA activation by inhibition of isoprenylcysteine-O-carboxyl methyltransferase. In the current study, we tested the effect of elevated adenosine on pulmonary endothelial barrier function in vitro and in vivo. We noted that adenosine alone dose dependently enhanced endothelial barrier function. While adenosine receptor A1 or A3 antagonists were ineffective, an adenosine transporter inhibitor, NBTI, or a combination of DPMX and MRS1754, antagonists for adenosine receptors A2A and A2B, respectively, partially attenuated the barrier-enhancing effect of adenosine. Similarly, inhibition of both A2A and A2B receptors with siRNA also blunted the effect of adenosine on barrier function. Interestingly, inhibition of both transporters and A2A/A2B receptors completely abolished adenosine-induced endothelial barrier enhancement. The adenosine receptor A2A and A2B agonist, NECA, also significantly enhanced endothelial barrier function. These data suggest that both adenosine transporters and A2A and A2B receptors are necessary for exerting maximal effect of adenosine on barrier enhancement. We also found that adenosine enhanced Rac1 GTPase activity and overexpression of dominant negative Rac1 attenuated adenosine-induced increases in focal adhesion complexes. We further demonstrated that elevation of cellular adenosine by inhibition of adenosine deaminase with Pentostatin significantly enhanced endothelial basal barrier function, an effect that was also associated with enhanced Rac1 GTPase activity and with increased focal adhesion complexes and adherens junctions. Finally, using a non-inflammatory acute lung injury (ALI) model induced by α-naphthylthiourea, we found that administration of Pentostatin, which elevated lung adenosine level by 10-fold, not only attenuated the development of edema before ALI but also partially reversed edema after ALI. The data suggest that adenosine deaminase inhibition may be useful in treatment of pulmonary edema in settings of ALI.
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Dissertations / Theses on the topic "Adenosine A2B receptor"

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BARALDI, Stefania. "Design and Synthesis of New A2B Adenosine Receptor Antagonists." Doctoral thesis, Università degli studi di Ferrara, 2009. http://hdl.handle.net/11392/2388704.

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Starting from chemical structure of N-benzo-[1,3]dioxol-5-yl-2-[5-(2,6dioxo-1,3-dipropyl-2,3,6,7-tetrahydro-1H-purin-8-yl)-1-methyl-1H-pyrazol3-yloxy]-acetamide, MRE2029F20* various structural modifications were realized to afford a new series of A2B antagonists. The bioisosteric replacement of the anilide moiety with benzimidazole or quinazoline rings, the effect of the substitution of pyrazole with isoxazole moiety were investigated. Amide bond has been also replaced with the 5phenyl-1,2,4-oxadiazole nucleus on the basis of other adenosine pharmacophores reported previously. In this context the effect of the nitrogen at the 9-position has been also studied preparing four 9-deaza direct analogs of 8pyrazol-xanthine compounds to compare affinity and selectivity at A2B adenosine receptor. The most significant result was obtained by bioisosteric replacement of the anilide moiety with benzimidazole, achieving antagonists with high affinity and selectivity toward the A2BAR. In particular compound 8-[5-(4-Chloro-6-trifluoromethyl-1H-benzoimidazol-2-ylmethoxy)-2methyl-2H-pyrazol-3-yl]-1,3-dipropyl-3,7-dihydro-purine-2,6-dione (hA1 Ki = 2530 nM, hA2A Ki > 1000 nM, hA2B Ki = 9.4 nM, hA3 Ki > 1000 nM) and compound 8-[5-(4,6-Bis-trifluoromethyl-1H-benzoimidazol-2-ylmethoxy)-2methyl-2H-pyrazol-3-yl]-1,3-dipropyl-3,7 dihydro-purine-2,6-dione (hA1 Ki = 4462 nM, hA2A Ki > 1000 nM, hA2B Ki = 25 nM, hA3 Ki > 1000 nM), showed the best biological data. These new selective and potent A2B antagonists will aid in the elucidation of the physiological role of this receptor and possibily lead to therapeutilally useful agents for treating asthma, diabetes and other diseases.
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Sun, Fengqiang. "Physical and functional interaction of A2B adenosine receptor with alpha-actinin-1/." View abstract or full-text, 2009. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202009%20SUN.

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Johnston-Cox, Hillary A. "Control of vascular disease and glucose and insulin homeostasis by the A2b adenosine receptor." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12433.

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Thesis (Ph.D.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Cardiovascular disease remains a leading cause of mortality. Risk factors, including poor glycemic control, central obesity and dyslipidemia contribute to prothrombotic and proinflammatory states, which elevate the risk for adverse cardiovascular events. Identifying new pharmacological targets for glycemic control is essential for prevention and management of cardiovascular disease. Adenosine is an endogenous purine nucleoside released from various tissues following stress, or produced externally by ecto-nucleotidases. Adenosine modulates inflammation and influences the metabolic state. There are four adenosine receptors classified as adenylyl cyclase activating (A2a and A2b) or inhibiting (A1 and A3). Using an A2b adenosine receptor (A2bAR) knockout (KO) mouse, our laboratory previously showed that A2bAR protects against atherosclerosis. Subjecting A2bAR, Apolipoprotein E (ApoE) double KO mice to a high fat diet (HFD) led to augmented liver levels of the transcription factor sterol response element binding protein-1 (SREBP-1) and its downstream targets, cholesterol and triglycerides, as well as to increased atherosclerosis, compared to mice with normal A2bAR. The studies in this thesis showed that selective restoration of hepatic A2bAR by adenovirus mediated gene transfer, or in vivo administration of an A2bAR agonist, BAY 60-6853, reduced the lipid profile and atherosclerosis. This study identified the A2bAR as a therapeutic target for hyperlipidemia and atherosclerosis. Liver steatosis is often associated with impaired hepatic insulin signaling. To test the hypothesis that A2bAR controls glucose/insulin homeostasis, A2bAR KO mice, with normal ApoE background, were subjected to HFD. Compared to control mice, A2bAR KO mice developed obesity and hallmarks of type 2 diabetes (T2D). We identified a novel link between expression of A2bAR and insulin receptor substrate 2 (IRS-2). IRS-2 is downregulated and insulin signaling is impaired in tissues of A2bAR KO mice that exhibit a greater inflammatory state. Importantly, pharmacological activation of A2bAR under HFD, using BAY 60-6583, restored IRS-2 levels, and ameliorated T2D. In obese human subjects, A2bAR expression correlated strongly with IRS-2 expression. Taken together, our study identifies the A2bAR as a significant regulator of HFD-induced hallmarks of atherosclerosis and T2D, with dysregulated liver A2bAR expression being a common denominator. Our study points to A2bAR as a therapeutic target for these disorders.
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Afzal, Aqeela. "Reduction in pre-retinal neovascularization by ribozymes that cleave the A2B receptor mRNA." [Gainesville, Fla.] : University of Florida, 2003. http://purl.fcla.edu/fcla/etd/UFE0000624.

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Carroll, Shannon H. "The role of the A2B adenosine receptor in the differentiation of mesenchymal stem cells to osteoblasts and chondrocytes: implications for bone development and fracture repair." Thesis, Boston University, 2013. https://hdl.handle.net/2144/10953.

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Thesis (Ph.D.)--Boston University
The development, maintenance and repair of the skeletal system are dependent on the differentiation of both chondrocytes and osteoblasts from their common progenitor, the mesenchymal stem cell (MSC). The A2B adenosine receptor (A2BAR) is a G-protein-coupled receptor that signals by increasing cAMP and/or activating phospholipase C signaling. Considering the published roles of cAMP on MSC differentiation, and our finding that the expression of the A2BAR is induced following injury, we hypothesized that ablation or activation of the A2BAR impacts the differentiation of osteoblasts and chondrocytes and that this would manifest as changes in skeletal development and bone fracture repair. Activation of the A2BAR increased the differentiation of bone marrow-derived MSCs to osteoblasts by increasing mRNA expression of the transcription factors runt-related transcription factor 2 (Runx2) and Sp7 transcription factor (Osterix), which are essential for osteoblast differentiation. To examine the effect of the A2BAR on bone formation in vivo, we subjected wild type (WT) and A2BAR knockout (KO) mice to bone fracture. A2BAR KO mice had impaired bone formation during fracture repair with increased cartilage volume. As fracture repair recapitulates the events that occur during endochondral ossification, we compared the growth plates of WT and A2BAR KO mice. In comparison to WT, A2BAR KO mice had a shorter growth plate initially, but a taller growth plate at a later age. These results suggest that initiation of endochondral ossification may be delayed in the A2BAR KO mice. Finally, we investigated whether the A2BAR is involved in chondrocyte differentiation. A2BAR activation decreased mRNA expression of the key transcription factor for chondrocyte differentiation, SRY (sex-determining region Y)-box 9 (Sox9) and decreased the mRNA expression of the hypertrophic chondrocyte marker Collagen X. Taken together, these data demonstrate a previously unidentified role of the A2BAR receptor in regulating MSC differentiation to both osteoblast and chondrocyte lineages. Further, we showed that mice null for the A2BAR have dysregulated bone formation during development and after injury. The importance of this receptor during bone formation and fracture repair could have implications for A2BAR-based therapies for bone maintenance and repair.
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FANG, YING. "SIGNALING PATHWAY FROM THE A2B ADENOSINE RECEPTOR TO EXTRACELLULAR SIGNAL REGULATED KINASES (ERK1/2) IN HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS (HUVEC) AND ITS ROLE IN HUVEC PROLIFERATION." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148392082.

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Sorrentino, Claudia. "Role of CD73 - A2A/A2B receptors axis in cancer." Doctoral thesis, Universita degli studi di Salerno, 2018. http://hdl.handle.net/10556/3116.

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2016 - 2017
The adenosinergic pathway plays a critical role in cancer development and progression, as well as in drug resistance to chemotherapy and/or targeted-therapy. The goal of this PhD thesis was to investigate and fully characterize the role of CD73/adenosine A2A-A2B receptors axis in cancer, highlighting the therapeutic potential of inhibitors of the adenosinergic pathway. We firstly characterized the mechanism/s by which A2BR promotes immunosuppression and angiogenesis in tumor-bearing hosts, focusing on the role of myeloid-derived suppressor cells (MDSCs) and cancer-associated fibroblasts (CAFs). The results revealed that treatment of melanoma-bearing mice with Bay60-6583, a selective A2BR agonist, is associated with 1. increased tumor VEGF-A expression and vessel density, and 2. increased accumulation of tumor-infiltrating CD11b+Gr1+cells (MDSCs). MDSCs strongly contribute to the immunosuppressive and angiogenic effects of Bay60-6583. Melanoma-bearing mice treated with a selective A2BR antagonist PSB1115 showed reduced tumor growth compared to controls and this effect was associated with reduced tumor angiogenesis, low levels of MDSCs and increased number of tumor-infiltrating CD8+ T cells. Furthermore, blockade of A2BR increased the anti-tumor effects of VEGF-A inhibitors. Next, we verified that A2BR activation also drives fibroblasts activation within melanoma tissues, by increasing the number of FAP positive cells within tumor lesions. FAP is a common marker of activated fibroblasts also named cancer-associated fibroblasts. These cells produce and secrete various tumor-promoting factors, including fibroblast growth factor (FGF)-2 and CXCL12 or stromal-derived factor 1 α (SDF1α), that were increased both in melanoma tissue and fibroblasts isolated from melanoma tissue or from skin upon Bay60-6583 treatment. Bay60-6583-induced FGF-2 from fibroblasts contributed to melanoma cells proliferation. The CXCL12/CXCR4 pathway, instead, was involved in the pro-angiogenic effects of A2BR agonist, but not in its immunosuppressive effects. These effects were significantly blocked by the A2BR antagonists PSB1115. Taken together, these data elucidate the pivotal role of A2BR in establishing a positive cross-talk between tumor-infiltrating immune cells, fibroblasts and endothelial cells that sustain tumor growth, reinforcing the therapeutic potential of A2BR blockers for cancer therapy. ... [edited by Author]
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Matsumoto, João Paulo de Pontes. "Efeito modulatório da nicotina sobre o receptor de adenosina A2a em cultura de células do bulbo de ratos geneticamente hipertensos e normotensos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-19022009-104148/.

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A hipertensão arterial é um problema de saúde pública no Brasil, pois aproximadamente 20 % da população adulta desenvolve hipertensão essencial, cujas causas ainda não são conhecidas. No entanto, sua gênese pode estar relacionada com disfunção nas áreas do sistema nervoso central (SNC) que regulam o sistema cardiovascular. O núcleo do trato solitário (NTS) e o bulbo ventrolateral são áreas importantes no controle neural da pressão arterial. Os receptores de adenosina A2a (rA2a) são encontrados em todo o SNC e estão relacionados com estudos terapêuticos de diversas doenças. No NTS a estimulação dos rA2a provoca ajustes pontuais em outros sistemas de neurotransmissão, além de diminuir a pressão arterial. A nicotina é uma molécula com uma vasta faixa de efeitos modulatórios em nosso organismo. Entre esses efeitos se destacam a capacidade de interagir com diversos sistemas de neurotransmissão nas áreas do bulbo relacionadas com a regulação da pressão arterial e de antecipar e/ou intensificar o desenvolvimento da hipertensão em sujeitos com pré-disposição genética. Desta forma, o objetivo do presente trabalho é avaliar o efeito modulatório da nicotina sobre o rA2a em cultura mista de neurônios e células gliais da porção dorso-medial do bulbo de ratos geneticamente hipertenso (SHR) e normotensos (WKY). Para isso, utilizaram-se técnicas como a de PCR em tempo real, Western Blotting e análise de ligação do receptor. Nossos resultados demonstraram que: 1) em condição basal células de ratos normotensos apresentam maior ligação do rA2a do que células de ratos hipertensos; 2) tratamento com nicotina resultou na diminuição da ligação do receptor em ambas as cepas, com um efeito de maior magnitude em células de ratos WKY; 3) nas duas linhagens o tratamento com nicotina alterou os níveis protéicos do rA2a, assim como o RNAm do receptor; 4) a linhagem e o tratamento separadamente, como a interação entre ambos influenciaram na expressão do RNAm , níveis protéicos e ligação do rA2a nas células dos ratos WKY e SHR. Por fim, os resultados apresentados aqui indicam que o rA2a em células de ratos hipertensos tem sua função deprimida em comparação com as células de ratos normotensos; e que a nicotina foi capaz de modular o funcionamento do rA2a, o qual pode influenciar no controle da pressão arterial. Esses dados são bastante interessantes, pois abrem novas perspectivas de análise dos mecanismos intracelulares envolvidos na modulação dos rA2a pela nicotina, assim como a importância desse sistema no desenvolvimento da hipertensão
Hypertension is one of the most common worldwide diseases afflicting humans. Because of the associated with morbidity and mortality and the cost to the society, it became an important public health challenge in Brazil. The mechanisms involved in development of hypertension still remain unclear However, hypertension can result from neuronal network imbalance in areas of the central nervous system that control blood pressure. The nucleus tractus solitarius (NTS) plays an important role in cardiovascular control. Within the NTS there are several neurotransmitters and neuromodulatory substances, such as adenosine, which acts on purinoreceptors A2a (A2ar). The A2ar modulates neurotransmission in the NTS and its activation may induce decrease in blood pressure by different mechanisms. Nicotine is a molecule that cross the blood-brain barrier and acts in several areas of central nervous system including the NTS. In this nucleus, nicotine is able to interact with some neurotransmitter systems and contributes for the development of hypertension in subjects with genetic predisposition to this disease. The goal of this study was to analyze the modulatory effects of nicotine on A2ar in cultured neurons and glial cells from medulla oblongata of normotensive (WKY) and spontaneously hypertensive rats (SHR). By means of real time PCR, Western Blotting and binding receptor assay. We have demonstrated that in basal condition cells of WKY presents increased binding of A2ar than the cells of SHR. Nicotine treatment induced a decrease in the binding of A2ar in both strains, however, this response was more pronounced in cells of WKY than SHR. Changes in mRNA and protein levels of A2ar was also observed in response to nicotine treatment. The strains and treatment separately, as well as the interaction between them influenced mRNA expression, protein level and binding of A2ar in NTS cells of WKY and SHR rats. Finally, these results show for the first time changes in A2ar mRNA expression, protein level and binding in cells from the medulla oblongata of WKY and SHR rats, as well as, the nicotine modulation upon this system, which might influence cardiovascular control. These data open up new approaches for the study of intracellular mechanisms involved in the modulation of adenosine A2a receptor by nicotine, as well as the importance of this interaction in the development of hypertension.
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Gandía, Sánchez Jorge. "Oligomerización del receptor A2A de adenosina: interpretando el receptorsoma." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/134352.

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Los receptores acoplados a proteína G (GPCR) conforman la familia de receptores de membrana más grande. El numeroso y variado tipo de señales que detectan han otorgado a estos receptores un alto interés farmacológico. Además, las interacciones entre diferentes tipos de GPCR formando complejos oligoméricos dan lugar a complejos con características bioquímicas diferenciadas de los protómeros que los forman. En esta Tesis Doctoral se han estudiado diferentes aspectos derivados este tipo de interacciones, centrando estos experimentos alrededor del receptor A2A de adenosina (A2AR), un importante neuromodulador del Sistema Nervioso Central. Por una parte, mediante la combinación de las técnicas de transferencia de energía resonante bioluminiscente (BRET) y de complementación bimolecular fluorescente (BiFC) se ha podido detectar in vivo que A2AR forma oligómeros con más de dos protómeros, tanto de tipo homomérico (Gandía et al., 2008) como heteromérico. En este último caso, se ha estudiado en concreto el oligómero de A2AR con el receptor D2 de dopamina y el receptor metabotrópico 5 de glutamato (Cabello et al., 2009). A continuación, se ha aplicado una variante de la técnica de doble híbrido específica para proteínas de membrana (MYTH), con la intención de detectar proteínas interaccionantes con A2AR. Gracias a esta aproximación, se han encontrado nuevas proteínas candidatas a interaccionar con nuestro receptor, destacando entre ellas un GPCR huérfano, GPR37. Mediante técnicas físicas y funcionales en modelos de cultivo celular y animales se ha podido validar la interacción A2AR/GPR37 y se ha comprobado que la presencia de GPR37 modifica la funcionalidad del receptor A2A de adenosina. Finalmente, para profundizar en las características estructurales de GPR37, poco conocidas hasta el momento, se ha estudiado la cola C-terminal del receptor. Así, se ha visto que existe una región rica en residuos de cisteína que regula el tráfico del receptor hacia la membrana plasmática. Además, este dominio rico en cisteínas modula el estrés de retículo endoplasmático generado al sobreexpresar GPR37 en cultivo celular y también la inducción de vías apoptóticas (actividad de caspasa-3) en estas mismas condiciones (Gandía et al., 2013).
G protein-coupled receptors (GPCR) consitute the biggest family of membrane receptors. Since they detect a large and diverse number of signals, they have a growing pharmacological interest. Furthermore, the interactions between different types of GPCR form oligomeric complexes that show different biochemical properties than the protomers they are made of. Different aspects of these interactions have been studied in this Doctoral Thesis, focusing the experiments around the adenosine A2A receptor, being adenosine an important modulator of the Central Nervous System. Firstly, by means of the combination of the bioluminescent ressonant energy transfer (BRET) and bimolecular fluorescent combination (BiFC) techniques we have detected in vivo that A2AR is able to form oligomers made up of more than two protomers, leading to homomeric complexes (Gandía et al., 2008) as well as others of heteromeric nature. In this latter case, we have studied the oligomer of A2AR with the dopamine D2 and glutamate metabotropic 5 receptors (Cabello et al., 2009). Following these experiments, we have applied a modified version of the yeast two-hybrid technique set up for membrane proteins (MYTH) in order to detect A2AR-interacting proteins. Thanks to this approach, we have found new potential interactors, and among them an orphan GPCR has stood out: GPR37. By means of physical and functional techniques in cell culture and animal models we have validated the A2AR/GPR37 interaction and we have demonstrated that the presence of GPR37 modifies the functionality of A2AR. Finally, in order to better understand the rather less studied structural characteristics of GPR37, we have studied its C-terminal tail. Thus, we have observed the presence of a cysteine-rich region that regulates the trafficking of the receptor to the plasma membrane. Furthermore, this cystein-rich domain modulates the GPR37-dependent endoplasmic reticulum stress, as well as the induction of apoptotic pathways (capase-3 activity) (Gandía et al., 2013).
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10

Larner, Carrie Jayne Byrom. "Selective targeting of the adenosine A2A receptor." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608592.

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Books on the topic "Adenosine A2B receptor"

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Chen, Jiang-Fan, and Akihisa Mori. Adenosine A2A Receptor Antagonists. Elsevier Science & Technology Books, 2023.

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Book chapters on the topic "Adenosine A2B receptor"

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Kalla, Rao V., Jeff Zablocki, Mojgan Aghazadeh Tabrizi, and Pier Giovanni Baraldi. "Recent Developments in A2B Adenosine Receptor Ligands." In Adenosine Receptors in Health and Disease, 99–122. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89615-9_4.

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Ghasemi, Fahimeh, Alireza Mehri, Jorge Peña-García, Helena den-Haan, Alfonso Pérez-Garrido, Afshin Fassihi, and Horacio Péréz-Sánchez. "Improving Activity Prediction of Adenosine A2B Receptor Antagonists by Nonlinear Models." In Bioinformatics and Biomedical Engineering, 635–44. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16480-9_61.

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Müller, Christa E., Younis Baqi, Sonja Hinz, and Vigneshwaran Namasivayam. "Medicinal Chemistry of A2B Adenosine Receptors." In The Adenosine Receptors, 137–68. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90808-3_6.

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "Adenosine A2A Receptors." In Encyclopedia of Psychopharmacology, 29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1103.

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Ferré, Sergi, César Quiroz, Marco Orrú, Xavier Guitart, Seema Gulyani, Richard Allen, and Christopher J. Earley. "Role of Striatal A2A Receptor Subpopulations in Neurological Disorders." In Adenosine, 179–97. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_9.

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Baraldi, Stefania, Pier Giovanni Baraldi, Paola Oliva, Kiran S. Toti, Antonella Ciancetta, and Kenneth A. Jacobson. "A2A Adenosine Receptor: Structures, Modeling, and Medicinal Chemistry." In The Adenosine Receptors, 91–136. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90808-3_5.

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Shook, Brian C. "Adenosine A2A Receptor Antagonists." In Topics in Medicinal Chemistry, 1–42. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/7355_2014_67.

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Pinna, Annalisa, Nicola Simola, Lucia Frau, and Micaela Morelli. "Symptomatic and Neuroprotective Effects of A2A Receptor Antagonists in Parkinson’s Disease." In Adenosine, 361–84. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_18.

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Morelli, Micaela, Anna R. Carta, and Peter Jenner. "Adenosine A2A Receptors and Parkinson’s Disease." In Adenosine Receptors in Health and Disease, 589–615. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89615-9_18.

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Cristalli, Gloria, Christa E. Müller, and Rosaria Volpini. "Recent Developments in Adenosine A2A Receptor Ligands." In Adenosine Receptors in Health and Disease, 59–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-89615-9_3.

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Conference papers on the topic "Adenosine A2B receptor"

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Karmouty-Quintana, Harry, James D. West, Anna Hemnes, Timothy S. Blackwell, Hongyan Zhong, Dewan Zeng, Luiz Belardinelli, and Michael Blackburn. "The Adenosine A2B Receptor Modulates Pulmonary Hypertension Associated With Chronic Lung Disease." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3391.

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Gałęzowski, Michał, Katarzyna Dziedzic, Paulina Węgrzyn, Aniela Gołas, Magdalena Bońkowska, Karolina Grycuk, Mateusz Ogórek, et al. "Abstract 5555:In vivoandin vitrocharacterization of RVU330 best-in-class dual A2A/A2B adenosine receptor antagonist." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5555.

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Jang, Sunyoung, Seunah Jun, Hosun Lee, Yongtaek Lee, Joo-Yun Byun, Junghwa Park, Yu-Yon Kim, Young Gil Ahn, YoungHoon Kim, and Kwee Hyun Suh. "Abstract 1704: Discovery and characterization of a novel triple A1/A2a/A2b adenosine receptor antagonist for cancer immunotherapy." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1704.

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Zhang, Hui, Michael R. Blackburn, Daniel J. Schneider, DeAndre L. Bluitt, Justin C. Jarrell, Joseph Sisson, Todd A. Wyatt, and Diane S. Allen-Gipson. "Adenosine Activation Of A2B Receptor(s) Is Essential For Stimulated Epithelial Ciliary Motility And Clearance." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1229.

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Barletta, Kathryn E., R. E. Cagnina, Marie D. Burdick, Robert M. Strieter, Robert A. Figler, Joel Linden, and Borna Mehrad. "Absence Of The Adenosine A2B Receptor Protects Against Klebsiella Pneumonia By Enhancing Neutrophil Bactericidal Activity." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2496.

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Zhong, Hongyan, Luiz Belardinelli, and Dewan Zeng. "The Expression And Function Of Adenosine Receptor Subtypes In Primary Human Pulmonary Arterial Smooth Muscle Cells And Endothelial Cells - Potential Role Of A2B Adenosine Receptor In Pulmonary Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3459.

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Owen, Dwight, Lai Wei, Mikhail Dikov, Shankar Suman, Ruohan Wu, Joseph Amann, Catherine Schweitzer, et al. "585 Phase 1 dose escalation trial of the selective A2B adenosine receptor antagonist PBF-1129 in patients with metastatic non-small cell lung cancer (mNSCLC)." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0585.

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Ahmad, Aftab, Shama Ahmad, Stacy M. Miller, Joan E. Loader, Sarah A. Gebb, John M. Shannon, and Carl W. White. "Adenosine A2A Receptor Promotes Growth In Fetal Rat Lung Explants." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6396.

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

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Davis Hovda, ME, Y. Chu, JB Wisk, J. Cifuentes, KD Chason, X. Hua, and SL Tilley. "Ventilator-Induced Lung Injury in A2A and A3 Adenosine Receptor-Deficient Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3558.

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Reports on the topic "Adenosine A2B receptor"

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

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

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