Relevant bibliographies by topics / Cyclic dinucleotides

Academic literature on the topic 'Cyclic dinucleotides'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Cyclic dinucleotides"

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Foley, J. F. "Cyclic Dinucleotides Get Stung." Science Signaling 4, no. 197 (November 1, 2011): ec303-ec303. http://dx.doi.org/10.1126/scisignal.4197ec303.

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Luteijn, Rutger D., Shivam A. Zaver, Benjamin G. Gowen, Stacia K. Wyman, Nick E. Garelis, Liberty Onia, Sarah M. McWhirter, et al. "SLC19A1 transports immunoreactive cyclic dinucleotides." Nature 573, no. 7774 (September 11, 2019): 434–38. http://dx.doi.org/10.1038/s41586-019-1553-0.

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Guey, Baptiste, and Andrea Ablasser. "A carrier for cyclic dinucleotides." Nature Immunology 20, no. 11 (October 10, 2019): 1418–20. http://dx.doi.org/10.1038/s41590-019-0521-z.

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Maelfait, Jonathan, and Jan Rehwinkel. "RECONsidering Sensing of Cyclic Dinucleotides." Immunity 46, no. 3 (March 2017): 337–39. http://dx.doi.org/10.1016/j.immuni.2017.03.005.

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Tschowri, Natalia. "Cyclic Dinucleotide-Controlled Regulatory Pathways in Streptomyces Species." Journal of Bacteriology 198, no. 1 (July 27, 2015): 47–54. http://dx.doi.org/10.1128/jb.00423-15.

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The cyclic dinucleotides cyclic 3′,5′-diguanylate (c-di-GMP) and cyclic 3′,5′-diadenylate (c-di-AMP) have emerged as key components of bacterial signal transduction networks. These closely related second messengers follow the classical general principles of nucleotide signaling by integrating diverse signals into regulatory pathways that control cellular responses to changing environments. They impact distinct cellular processes, with c-di-GMP having an established role in promoting bacterial adhesion and inhibiting motility and c-di-AMP being involved in cell wall metabolism, potassium homeostasis, and DNA repair. The involvement of c-dinucleotides in the physiology of the filamentous, nonmotile streptomycetes remained obscure until recent discoveries showed that c-di-GMP controls the activity of the developmental master regulator BldD and that c-di-AMP determines the level of the resuscitation-promoting factor A(RpfA) cell wall-remodelling enzyme. Here, I summarize our current knowledge of c-dinucleotide signaling inStreptomycesspecies and highlight the important roles of c-di-GMP and c-di-AMP in the biology of these antibiotic-producing, multicellular bacteria.
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Tosolini, Marie, Frédéric Pont, Delphine Bétous, Emmanuel Ravet, Laetitia Ligat, Frédéric Lopez, Mary Poupot, et al. "Human Monocyte Recognition of Adenosine-Based Cyclic Dinucleotides Unveils the A2a GαsProtein-Coupled Receptor Tonic Inhibition of Mitochondrially Induced Cell Death." Molecular and Cellular Biology 35, no. 2 (November 10, 2014): 479–95. http://dx.doi.org/10.1128/mcb.01204-14.

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Cyclic dinucleotides are important messengers for bacteria and protozoa and are well-characterized immunity alarmins for infected mammalian cells through intracellular binding to STING receptors. We sought to investigate their unknown extracellular effects by adding cyclic dinucleotides to the culture medium of freshly isolated human blood cellsin vitro. Here we report that adenosine-containing cyclic dinucleotides induce the selective apoptosis of monocytes through a novel apoptotic pathway. We demonstrate that these compounds are inverse agonist ligands of A2a, a Gαs-coupled adenosine receptor selectively expressed by monocytes. Inhibition of monocyte A2a by these ligands induces apoptosis through a mechanism independent of that of the STING receptors. The blockade of basal (adenosine-free) signaling from A2a inhibits protein kinase A (PKA) activity, thereby recruiting cytosolic p53, which opens the mitochondrial permeability transition pore and impairs mitochondrial respiration, resulting in apoptosis. A2a antagonists and inverse agonist ligands induce apoptosis of human monocytes, while A2a agonists are antiapoptotic.In vivo, we used a mock developing human hematopoietic system through NSG mice transplanted with human CD34+cells. Treatment with cyclic di-AMP selectively depleted A2a-expressing monocytes and their precursors via apoptosis. Thus, monocyte recognition of cyclic dinucleotides unravels a novel proapoptotic pathway: the A2a Gαsprotein-coupled receptor (GPCR)-driven tonic inhibitory signaling of mitochondrion-induced cell death.
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López-Villamizar, Iralis, Alicia Cabezas, Rosa María Pinto, José Canales, João Meireles Ribeiro, Joaquim Rui Rodrigues, María Jesús Costas, and José Carlos Cameselle. "Molecular Dissection of Escherichia coli CpdB: Roles of the N Domain in Catalysis and Phosphate Inhibition, and of the C Domain in Substrate Specificity and Adenosine Inhibition." International Journal of Molecular Sciences 22, no. 4 (February 17, 2021): 1977. http://dx.doi.org/10.3390/ijms22041977.

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CpdB is a 3′-nucleotidase/2′3′-cyclic nucleotide phosphodiesterase, active also with reasonable efficiency on cyclic dinucleotides like c-di-AMP (3′,5′-cyclic diadenosine monophosphate) and c-di-GMP (3′,5′-cyclic diadenosine monophosphate). These are regulators of bacterial physiology, but are also pathogen-associated molecular patterns recognized by STING to induce IFN-β response in infected hosts. The cpdB gene of Gram-negative and its homologs of gram-positive bacteria are virulence factors. Their protein products are extracytoplasmic enzymes (either periplasmic or cell–wall anchored) and can hydrolyze extracellular cyclic dinucleotides, thus reducing the innate immune responses of infected hosts. This makes CpdB(-like) enzymes potential targets for novel therapeutic strategies in infectious diseases, bringing about the necessity to gain insight into the molecular bases of their catalytic behavior. We have dissected the two-domain structure of Escherichia coli CpdB to study the role of its N-terminal and C-terminal domains (CpdB_Ndom and CpdB_Cdom). The specificity, kinetics and inhibitor sensitivity of point mutants of CpdB, and truncated proteins CpdB_Ndom and CpdB_Cdom were investigated. CpdB_Ndom contains the catalytic site, is inhibited by phosphate but not by adenosine, while CpdB_Cdom is inactive but contains a substrate-binding site that determines substrate specificity and adenosine inhibition of CpdB. Among CpdB substrates, 3′-AMP, cyclic dinucleotides and linear dinucleotides are strongly dependent on the CpdB_Cdom binding site for activity, as the isolated CpdB_Ndom showed much-diminished activity on them. In contrast, 2′,3′-cyclic mononucleotides and bis-4-nitrophenylphosphate were actively hydrolyzed by CpdB_Ndom, indicating that they are rather independent of the CpdB_Cdom binding site.
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Luteijn, Rutger D., Shivam A. Zaver, Benjamin G. Gowen, Stacia K. Wyman, Nick E. Garelis, Liberty Onia, Sarah M. McWhirter, et al. "Author Correction: SLC19A1 transports immunoreactive cyclic dinucleotides." Nature 579, no. 7800 (March 2020): E12. http://dx.doi.org/10.1038/s41586-020-2064-8.

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Danilchanka, Olga, and John J. Mekalanos. "Cyclic Dinucleotides and the Innate Immune Response." Cell 154, no. 5 (August 2013): 962–70. http://dx.doi.org/10.1016/j.cell.2013.08.014.

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Gutten, Ondrej, Petr Jurečka, Zahra Aliakbar Tehrani, Miloš Buděšínský, Jan Řezáč, and Lubomír Rulíšek. "Conformational energies and equilibria of cyclic dinucleotides in vacuo and in solution: computational chemistry vs. NMR experiments." Physical Chemistry Chemical Physics 23, no. 12 (2021): 7280–94. http://dx.doi.org/10.1039/d0cp05993e.

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Dissertations / Theses on the topic "Cyclic dinucleotides"

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Smith, E. E. "Novel dinucleotides, precursors to fluorescent cyclic nucleotides." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487327.

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While the function of NAD+ as energy transducer has been well established, it is also now known to play an important role in cellular processes such as gene regulation and cell maintenance. In addition; NAD is a precursor to biologically active metabolites such as ADPR, ADP_ribosyl-derivatives and cADPR. cADPR is a Ca 2 -modulating second messenger formed by the cyclisation of NAD+ by ADP-ribosyl cyclases. While three different enzymes have been identified as cyclases, the mechanism and site of activity of such enzymes has not yet been fully established. The aim of this work is thus to synthesise base-modified NAD+ analogues that can reach the cyclase active site, and be enzymatically converted to cyclic products that fluoresce at wavelengths not harmful to cells. Such analogues may facilitate establishing the location and mechanism of the cyclase and also the metabolic pathway of cADPR. Nine novel n~cleosides were synthesised by glycosylation of the selected heterocycles with a protected ribose using Vorbriiggen conditions. Subsequent phosphorylation using PM chemistry developed by Yoshikawa afforded the nucleotide analogues. Fluorescence studies of the nucleosides were then carried out to provide preliminary information as to whether any of the analogues would fluoresce, and at which excitation and emission wavelengths the fluorescence would occur. This synthetic route was designed to introduce the relatively unstable nicotinamide moiety at the final step. However, coupling to nicotinamide mononucleotide to form the cyclic precursors proved unfruitful, despite subjection to numerous different reaction conditions.
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Smyth, Lisa M. "The nicotinamide adenine dinucleotide (NAD)/cyclic ADP-ribose/ADP-ribose system, new to the peripheral synapse." abstract and full text PDF (free order & download UNR users only), 2005. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3210943.

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Collins, Thomas Peter. "Regulation of atrial myocyte calcium signalling by second messengers including cyclic AMP, Inositol trisphosphate and nicotinic acid adenine dinucleotide phosphate." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510944.

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Noriega, Esteban Núria. "The Rtg1 and Rtg3 proteins are novel transcription factors regulated by the yeast hog1 mapk upon osmotic stress." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7158.

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La adaptación de la levadura Saccharomyces cerevisiae a condiciones de alta osmolaridad está mediada por la vía de HOG ((high-osmolarity glycerol). La activación de esta vía induce una serie de respuestas que van a permitir la supervivencia celular en respuesta a estrés. La regulación génica constituye una respuesta clave para dicha supervivencia. Se han descrito cinco factores de transcripción regulados por Hog1 en respuesta a estrés osmótico. Sin embargo, éstos no pueden explicar la totalidad de los genes regulados por la MAPK Hog1. En el presente trabajo describimos cómo el complejo transcripcional formado por las proteínas Rtg1 y Rtg3 regula, a través de la quinasa Hog1, la expresión de un conjunto específico de genes. Hog1 fosforila Rtg1 y Rtg3, aunque ninguna de estas fosforilaciones son esenciales para regulación transcripcional en respuesta a estrés. Este trabajo también muestra cómo la deleción de proteínas RTG provoca osmosensibilidad celular, lo que indica que la integridad de la vía de RTG es esencial para la supervivencia celular frente a un estrés osmótico.
In Saccharomyces cerevisiae the adaptation to high osmolarity is mediated by the HOG (high-osmolarity glycerol) pathway, which elicits different cellular responses required for cell survival upon osmostress. Regulation of gene expression is a major adaptative response required for cell survival in response to osmotic stress. At least five transcription factors have been reported to be controlled by the Hog1 MAPK. However, they cannot account for the regulation of all of the genes under the control of the Hog1 MAPK. Here we show that the Rtg1/3 transcriptional complex regulates the expression of specific genes upon osmostress in a Hog1-dependent manner. Hog1 phosphorylates both Rtg1 and Rtg3 proteins. However, none of these phosphorylations are essential for the transcriptional regulation upon osmostress. Here we also show that the deletion of RTG proteins leads to osmosensitivity at high osmolarity, suggesting that the RTG-pathway integrity is essential for cell survival upon stress.
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Vendrell, Arasa Alexandre. "SCF cdc4 regulates msn2 and msn4 dependent gene expression to counteract hog1 induced lethality." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7153.

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L'activació sostinguda de Hog1 porta a una inhibició del creixement cel·lular. En aquest treball, hem observat que el fenotip de letalitat causat per l'activació sostinguda de Hog1 és parcialment inhibida per la mutació del complexe SCFCDC4. La inhibició de la mort causada per l'activació sostinguda de Hog1 depèn de la via d'extensió de la vida. Quan Hog1 s'activa de manera sostinguda, la mutació al complexe SCFCDC4 fa que augmenti l'expressió gènica depenent de Msn2 i Msn4 que condueix a una sobreexpressió del gen PNC1 i a una hiperactivació de la deacetilassa Sir2. La hiperactivació de Sir2 és capaç d'inhibir la mort causada per l'activació sostinguda de Hog1.
També hem observat que la mort cel·lular causada per l'activació sostinguda de Hog1 és deguda a una inducció d'apoptosi. L'apoptosi induïda per Hog1 és inhibida per la mutació al complexe SCFCDC4. Per tant, la via d'extensió de la vida és capaç de prevenir l'apoptosi a través d'un mecanisme desconegut.
Sustained Hog1 activation leads to an inhibition of cell growth. In this work, we have observed that the lethal phenotype caused by sustained Hog1 activation is prevented by SCFCDC4 mutants. The prevention of Hog1-induced cell death by SCFCDC4 mutation depends on the lifespan extension pathway. Upon sustained Hog1 activation, SCFCDC4 mutation increases Msn2 and Msn4 dependent gene expression that leads to a PNC1 overexpression and a Sir2 deacetylase hyperactivation. Then, hyperactivation of Sir2 is able to prevent cell death caused by sustained Hog1 activation.
We have also observed that cell death upon sustained Hog1 activation is due to an induction of apoptosis. The apoptosis induced by Hog1 is decreased by SCFCDC4 mutation. Therefore, lifespan extension pathway is able to prevent apoptosis by an unknown mechanism.
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Book chapters on the topic "Cyclic dinucleotides"

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Orr, Mona W., and Vincent T. Lee. "Enzymatic Degradation of Linear Dinucleotide Intermediates of Cyclic Dinucleotides." In Microbial Cyclic Di-Nucleotide Signaling, 93–104. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33308-9_6.

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Du, Xiao-Xia, and Xiao-Dong Su. "Detection of Cyclic Dinucleotides by STING." In c-di-GMP Signaling, 59–69. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7240-1_6.

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Mankan, Arun K., Martina Müller, Gregor Witte, and Veit Hornung. "Cyclic Dinucleotides in the Scope of the Mammalian Immune System." In Non-canonical Cyclic Nucleotides, 269–89. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/164_2016_5002.

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Burhenne, Heike, and Volkhard Kaever. "Quantification of Cyclic Dinucleotides by Reversed-Phase LC-MS/MS." In Cyclic Nucleotide Signaling in Plants, 27–37. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-441-8_3.

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Petchiappan, Anushya, Avisek Mahapa, and Dipankar Chatterji. "Cyclic Dinucleotide Signaling in Mycobacteria." In Microbial Cyclic Di-Nucleotide Signaling, 3–25. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33308-9_1.

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Lee, Vincent T. "Detection of Cyclic Dinucleotide Binding Proteins." In Microbial Cyclic Di-Nucleotide Signaling, 107–24. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33308-9_7.

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Sintim, Herman O., and Clement Opoku-Temeng. "Targeting Cyclic Dinucleotide Signaling with Small Molecules." In Microbial Cyclic Di-Nucleotide Signaling, 577–91. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33308-9_33.

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Schwede, Frank, Hans-Gottfried Genieser, and Andreas Rentsch. "The Chemistry of the Noncanonical Cyclic Dinucleotide 2′3′-cGAMP and Its Analogs." In Non-canonical Cyclic Nucleotides, 359–84. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/164_2015_43.

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Graeff, Richard M., and Hon Cheung Lee. "Determination of ADP-Ribosyl Cyclase Activity, Cyclic ADP-Ribose, and Nicotinic Acid Adenine Dinucleotide Phosphate in Tissue Extracts." In Cyclic Nucleotide Signaling in Plants, 39–56. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-441-8_4.

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Maddess, Matthew, John McIntosh, and Wonsuk Chang. "Discovery and Chemical Development of Uvelostinag (MK-1454): A Therapeutic Cyclic Dinucleotide Agonist of the Stimulator of Interferon Gene." In ACS Symposium Series, 1–94. Washington, DC: American Chemical Society, 2022. http://dx.doi.org/10.1021/bk-2022-1423.ch001.

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Conference papers on the topic "Cyclic dinucleotides"

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Glickman, Laura Hix, David B. Kanne, Kelsey E. Gauthier, George E. Katibah, Justin J. Leong, Ken Metchette, Thomas W. Dubensky, and Sarah M. McWhirter. "Abstract 4272: Potentin situcancer immunotherapy with synthetic human STING-activating cyclic dinucleotides." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4272.

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Fu, Juan, Qi Zhen, Drew Pardoll, Tom Dubensky, and Young Kim. "Abstract B42: Cyclic dinucleotides (CDNs) activated DC and NK cells in antitumor immunotherapy." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b42.

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Dubensky, Thomas W., Meredith L. Leong, David B. Kanne, Edward E. Lemmens, Ken Metchette, Weiqun Liu, Marcella Fasso, et al. "Abstract 4573: STINGVAX - A novel tumor vaccine with cyclic dinucleotides - can induce potent anti-tumor responsesin vivo." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4573.

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Gadkaree, Shekhar K., Rupashree Sen, Juan Fu, Clint Allen, and Young J. Kim. "Abstract B087: Cyclic dinucleotide: A novel adjuvant for squamous cell carcinoma." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b087.

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Glickman, Laura Hix, Leticia Corrales, Sarah M. McWhirter, David B. Kanne, Kelsey E. Sivick, Jason R. Baird, Edward Lemmens, et al. "Abstract IA10: Effective immunotherapy regimens incorporating highly active human STING-activating cyclic dinucleotide derivatives." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-ia10.

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Gremel, Gabriela, Maria A. Impagnatiello, Sebastian Carotta, Otmar Schaaf, Paolo M. Chetta, Thorsten Oost, Thomas Zichner, et al. "Abstract 4522: Potent induction of a tumor-specific immune response by a cyclic dinucleotide STING agonist." 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.am2020-4522.

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Glickman, Laura Hix, David B. Kanne, Sarah M. McWhirter, Meredith L. Leong, Edward E. Lemmens, Ken Metchette, Russell E. Vance, Drew M. Pardoll, and Thomas W. Dubensky. "Abstract 2566: Activation of tumor-initiated T cell priming and tumor destruction with potent STING-activating cyclic dinucleotide derivatives." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2566.

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McWhirter, Sarah M., Laura Hix Glickman, Tony Desbien, Kelsey Sivick Gauthier, David Kanne, Shailaja Kasibhatla, Jie Li, et al. "Abstract B020: STING activation in the tumor microenvironment using a synthetic human STING-activating cyclic dinucleotide induces potent antitumor immunity." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b020.

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Wang, Zezhou, Peter Dove, David Rosa, Bolette Bossen, Simone Helke, Marilyse Charbonneau, Laura Brinen, et al. "Abstract 3854: Preclinical characterization of a novel non-cyclic dinucleotide small molecule STING agonist with potent antitumor activity in mice." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3854.

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Wang, Zezhou, Peter Dove, David Rosa, Bolette Bossen, Simone Helke, Marilyse Charbonneau, Laura Brinen, et al. "Abstract 3854: Preclinical characterization of a novel non-cyclic dinucleotide small molecule STING agonist with potent antitumor activity in mice." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3854.

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