Littérature scientifique sur le sujet « Adenosine A2B receptor »
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Articles de revues sur le sujet "Adenosine A2B receptor"
Wolska, Nina, et Marcin Rozalski. « Blood Platelet Adenosine Receptors as Potential Targets for Anti-Platelet Therapy ». International Journal of Molecular Sciences 20, no 21 (3 novembre 2019) : 5475. http://dx.doi.org/10.3390/ijms20215475.
Texte intégralFeng, Ming-Guo, et L. Gabriel Navar. « Afferent arteriolar vasodilator effect of adenosine predominantly involves adenosine A2B receptor activation ». American Journal of Physiology-Renal Physiology 299, no 2 (août 2010) : F310—F315. http://dx.doi.org/10.1152/ajprenal.00149.2010.
Texte intégralGebremedhin, Debebe, Brian Weinberger, David Lourim et David R. Harder. « Adenosine Can Mediate its Actions through Generation of Reactive Oxygen Species ». Journal of Cerebral Blood Flow & ; Metabolism 30, no 10 (9 juin 2010) : 1777–90. http://dx.doi.org/10.1038/jcbfm.2010.70.
Texte intégralZaynagetdinov, 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 (15 juin 2022) : 3499. http://dx.doi.org/10.1158/1538-7445.am2022-3499.
Texte intégralXaus, Jordi, Maribel Mirabet, Jorge Lloberas, Concepció Soler, Carme Lluis, Rafael Franco et Antonio Celada. « IFN-γ Up-Regulates the A2B Adenosine Receptor Expression in Macrophages : A Mechanism of Macrophage Deactivation ». Journal of Immunology 162, no 6 (15 mars 1999) : 3607–14. http://dx.doi.org/10.4049/jimmunol.162.6.3607.
Texte intégralShi, Yanrong, Xiaoguang Liu, Debebe Gebremedhin, John R. Falck, David R. Harder et 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 (23 mai 2007) : 111–25. http://dx.doi.org/10.1038/sj.jcbfm.9600511.
Texte intégralMarquardt, D. L., L. L. Walker et S. Heinemann. « Cloning of two adenosine receptor subtypes from mouse bone marrow-derived mast cells. » Journal of Immunology 152, no 9 (1 mai 1994) : 4508–15. http://dx.doi.org/10.4049/jimmunol.152.9.4508.
Texte intégralDubey, Raghvendra K., Delbert G. Gillespie et Edwin K. Jackson. « A2B Adenosine Receptors Mediate the Anti-Mitogenic Effects of Adenosine in Cardiac Fibroblasts ». Hypertension 36, suppl_1 (octobre 2000) : 708. http://dx.doi.org/10.1161/hyp.36.suppl_1.708-b.
Texte intégralZhan, Enbo, Victoria J. McIntosh et 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 (septembre 2011) : H1183—H1189. http://dx.doi.org/10.1152/ajpheart.00264.2011.
Texte intégralLu, Qing, Elizabeth O. Harrington, Julie Newton, Brian Casserly, Gregory Radin, Rod Warburton, Yang Zhou, Michael R. Blackburn et 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 (juin 2010) : L755—L767. http://dx.doi.org/10.1152/ajplung.00330.2009.
Texte intégralThèses sur le sujet "Adenosine A2B receptor"
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.
Texte intégralSun, 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.
Texte intégralJohnston-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.
Texte intégralCardiovascular 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.
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.
Texte intégralCarroll, 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.
Texte intégralThe 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.
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.
Texte intégralSorrentino, Claudia. « Role of CD73 - A2A/A2B receptors axis in cancer ». Doctoral thesis, Universita degli studi di Salerno, 2018. http://hdl.handle.net/10556/3116.
Texte intégralThe 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/.
Texte intégralHypertension 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.
Gandía, Sánchez Jorge. « Oligomerización del receptor A2A de adenosina : interpretando el receptorsoma ». Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/134352.
Texte intégralG 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).
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.
Texte intégralLivres sur le sujet "Adenosine A2B receptor"
Chen, Jiang-Fan, et Akihisa Mori. Adenosine A2A Receptor Antagonists. Elsevier Science & Technology Books, 2023.
Trouver le texte intégralChapitres de livres sur le sujet "Adenosine A2B receptor"
Kalla, Rao V., Jeff Zablocki, Mojgan Aghazadeh Tabrizi et Pier Giovanni Baraldi. « Recent Developments in A2B Adenosine Receptor Ligands ». Dans 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.
Texte intégralGhasemi, Fahimeh, Alireza Mehri, Jorge Peña-García, Helena den-Haan, Alfonso Pérez-Garrido, Afshin Fassihi et Horacio Péréz-Sánchez. « Improving Activity Prediction of Adenosine A2B Receptor Antagonists by Nonlinear Models ». Dans Bioinformatics and Biomedical Engineering, 635–44. Cham : Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16480-9_61.
Texte intégralMüller, Christa E., Younis Baqi, Sonja Hinz et Vigneshwaran Namasivayam. « Medicinal Chemistry of A2B Adenosine Receptors ». Dans The Adenosine Receptors, 137–68. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90808-3_6.
Texte intégralScherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts et al. « Adenosine A2A Receptors ». Dans Encyclopedia of Psychopharmacology, 29. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1103.
Texte intégralFerré, Sergi, César Quiroz, Marco Orrú, Xavier Guitart, Seema Gulyani, Richard Allen et Christopher J. Earley. « Role of Striatal A2A Receptor Subpopulations in Neurological Disorders ». Dans Adenosine, 179–97. New York, NY : Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_9.
Texte intégralBaraldi, Stefania, Pier Giovanni Baraldi, Paola Oliva, Kiran S. Toti, Antonella Ciancetta et Kenneth A. Jacobson. « A2A Adenosine Receptor : Structures, Modeling, and Medicinal Chemistry ». Dans The Adenosine Receptors, 91–136. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90808-3_5.
Texte intégralShook, Brian C. « Adenosine A2A Receptor Antagonists ». Dans Topics in Medicinal Chemistry, 1–42. Cham : Springer International Publishing, 2014. http://dx.doi.org/10.1007/7355_2014_67.
Texte intégralPinna, Annalisa, Nicola Simola, Lucia Frau et Micaela Morelli. « Symptomatic and Neuroprotective Effects of A2A Receptor Antagonists in Parkinson’s Disease ». Dans Adenosine, 361–84. New York, NY : Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_18.
Texte intégralMorelli, Micaela, Anna R. Carta et Peter Jenner. « Adenosine A2A Receptors and Parkinson’s Disease ». Dans 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.
Texte intégralCristalli, Gloria, Christa E. Müller et Rosaria Volpini. « Recent Developments in Adenosine A2A Receptor Ligands ». Dans 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.
Texte intégralActes de conférences sur le sujet "Adenosine A2B receptor"
Karmouty-Quintana, Harry, James D. West, Anna Hemnes, Timothy S. Blackwell, Hongyan Zhong, Dewan Zeng, Luiz Belardinelli et Michael Blackburn. « The Adenosine A2B Receptor Modulates Pulmonary Hypertension Associated With Chronic Lung Disease ». Dans 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.
Texte intégralGałęzowski, 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 ». Dans 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.
Texte intégralJang, Sunyoung, Seunah Jun, Hosun Lee, Yongtaek Lee, Joo-Yun Byun, Junghwa Park, Yu-Yon Kim, Young Gil Ahn, YoungHoon Kim et Kwee Hyun Suh. « Abstract 1704 : Discovery and characterization of a novel triple A1/A2a/A2b adenosine receptor antagonist for cancer immunotherapy ». Dans 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.
Texte intégralZhang, Hui, Michael R. Blackburn, Daniel J. Schneider, DeAndre L. Bluitt, Justin C. Jarrell, Joseph Sisson, Todd A. Wyatt et Diane S. Allen-Gipson. « Adenosine Activation Of A2B Receptor(s) Is Essential For Stimulated Epithelial Ciliary Motility And Clearance ». Dans 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.
Texte intégralBarletta, Kathryn E., R. E. Cagnina, Marie D. Burdick, Robert M. Strieter, Robert A. Figler, Joel Linden et Borna Mehrad. « Absence Of The Adenosine A2B Receptor Protects Against Klebsiella Pneumonia By Enhancing Neutrophil Bactericidal Activity ». Dans 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.
Texte intégralZhong, Hongyan, Luiz Belardinelli et 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 ». Dans 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.
Texte intégralOwen, 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) ». Dans SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0585.
Texte intégralAhmad, Aftab, Shama Ahmad, Stacy M. Miller, Joan E. Loader, Sarah A. Gebb, John M. Shannon et Carl W. White. « Adenosine A2A Receptor Promotes Growth In Fetal Rat Lung Explants ». Dans 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.
Texte intégralLin, Juqiang, Yating Lin, Yiming Huang, Zhiwei Wu, Jianshu Xu, Ya Hu et Shusen Xie. « Quantitative FRET measurement of the interaction of A1 adenosine receptors and A2A adenosine receptors in living cell ». Dans Optics in Health Care and Biomedical Optics VIII, sous la direction de Qingming Luo, Xingde Li, Yuguo Tang et Ying Gu. SPIE, 2018. http://dx.doi.org/10.1117/12.2500692.
Texte intégralDavis Hovda, ME, Y. Chu, JB Wisk, J. Cifuentes, KD Chason, X. Hua et SL Tilley. « Ventilator-Induced Lung Injury in A2A and A3 Adenosine Receptor-Deficient Mice. » Dans 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.
Texte intégralRapports d'organisations sur le sujet "Adenosine A2B receptor"
Liou, Gregory I., Saif Ahmad, Mohammad Naime, Nadeem Fatteh et Sohail Khan. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA : Defense Technical Information Center, décembre 2012. http://dx.doi.org/10.21236/ada581642.
Texte intégralLiou, Gregory I., Saif Ahmad et Ahmed Elsherbini. Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies. Fort Belvoir, VA : Defense Technical Information Center, décembre 2013. http://dx.doi.org/10.21236/ada600384.
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