Relevant bibliographies by topics / Atypical Chemokine Receptors

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Academic literature on the topic 'Atypical Chemokine Receptors'

Author: Grafiati
Published: 2 November 2024
Last updated: 31 July 2025

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Journal articles on the topic "Atypical Chemokine Receptors"

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Hansell, C. A. H., C. V. Simpson, and R. J. B. Nibbs. "Chemokine sequestration by atypical chemokine receptors." Biochemical Society Transactions 34, no. 6 (2006): 1009–13. http://dx.doi.org/10.1042/bst0341009.

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Leucocyte migration is essential for robust immune and inflammatory responses, and plays a critical role in many human diseases. Chemokines, a family of small secreted protein chemoattractants, are of fundamental importance in this process, directing leucocyte trafficking by signalling through heptahelical G-protein-coupled receptors expressed by the migrating cells. However, several mammalian chemokine receptors, including D6 and CCX-CKR (ChemoCentryx chemokine receptor), do not fit existing models of chemokine receptor function, and do not even appear to signal in response to chemokine bindi
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Borroni, Elena M., Raffaella Bonecchi, and Annalisa M. VanHook. "Science Signaling Podcast: 30 April 2013." Science Signaling 6, no. 273 (2013): pc11. http://dx.doi.org/10.1126/scisignal.2004231.

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This Podcast features an interview with Elena M. Borroni and Raffaella Bonecchi, authors of a Research Article that appears in the 30 April 2013 issue of Science Signaling. Chemokines recruit leukocytes to sites of infection and inflammation by binding to chemokine receptors, which are members of the G protein–coupled receptor superfamily, present on the surface of leukocytes. Whereas activation of typical chemokine receptors leads to G protein–dependent signaling that promotes cell migration toward the chemokine source, activation of atypical chemokine receptors does not promote cell migratio
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Groblewska, Magdalena, Ala Litman-Zawadzka, and Barbara Mroczko. "The Role of Selected Chemokines and Their Receptors in the Development of Gliomas." International Journal of Molecular Sciences 21, no. 10 (2020): 3704. http://dx.doi.org/10.3390/ijms21103704.

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Among heterogeneous primary tumors of the central nervous system (CNS), gliomas are the most frequent type, with glioblastoma multiforme (GBM) characterized with the worst prognosis. In their development, certain chemokine/receptor axes play important roles and promote proliferation, survival, metastasis, and neoangiogenesis. However, little is known about the significance of atypical receptors for chemokines (ACKRs) in these tumors. The objective of the study was to present the role of chemokines and their conventional and atypical receptors in CNS tumors. Therefore, we performed a thorough s
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Ulvmar, Maria Helena, Elin Hub, and Antal Rot. "Atypical chemokine receptors." Experimental Cell Research 317, no. 5 (2011): 556–68. http://dx.doi.org/10.1016/j.yexcr.2011.01.012.

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Legler, Daniel F., and Marcus Thelen. "New insights in chemokine signaling." F1000Research 7 (January 23, 2018): 95. http://dx.doi.org/10.12688/f1000research.13130.1.

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Chemokine signaling is essential for coordinated cell migration in health and disease to specifically govern cell positioning in space and time. Typically, chemokines signal through heptahelical, G protein-coupled receptors to orchestrate cell migration. Notably, chemokine receptors are highly dynamic structures and signaling efficiency largely depends on the discrete contact with the ligand. Promiscuity of both chemokines and chemokine receptors, combined with biased signaling and allosteric modulation of receptor activation, guarantees a tightly controlled recruitment and positioning of indi
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Gencer, Selin, Emiel van der Vorst, Maria Aslani, Christian Weber, Yvonne Döring, and Johan Duchene. "Atypical Chemokine Receptors in Cardiovascular Disease." Thrombosis and Haemostasis 119, no. 04 (2019): 534–41. http://dx.doi.org/10.1055/s-0038-1676988.

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AbstractInflammation has been well recognized as one of the main drivers of atherosclerosis development and therefore cardiovascular diseases (CVDs). It has been shown that several chemokines, small 8 to 12 kDa cytokines with chemotactic properties, play a crucial role in the pathophysiology of atherosclerosis. Chemokines classically mediate their effects by binding to G-protein-coupled receptors called chemokine receptors. In addition, chemokines can also bind to atypical chemokine receptors (ACKRs). ACKRs fail to induce G-protein-dependent signalling pathways and thus subsequent cellular res
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Gustavsson, Martin, Douglas P. Dyer, Chunxia Zhao, and Tracy M. Handel. "Kinetics of CXCL12 binding to atypical chemokine receptor 3 reveal a role for the receptor N terminus in chemokine binding." Science Signaling 12, no. 598 (2019): eaaw3657. http://dx.doi.org/10.1126/scisignal.aaw3657.

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Chemokines bind to membrane-spanning chemokine receptors, which signal through G proteins and promote cell migration. However, atypical chemokine receptor 3 (ACKR3) does not appear to couple to G proteins, and instead of directly promoting cell migration, it regulates the extracellular concentration of chemokines that it shares with the G protein–coupled receptors (GPCRs) CXCR3 and CXCR4, thereby influencing the responses of these receptors. Understanding how these receptors bind their ligands is important for understanding these different processes. Here, we applied association and dissociati
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Pacheco, Messias Oliveira, Fernanda Agostini Rocha, Thiago Pinheiro Arrais Aloia, and Luciana Cavalheiro Marti. "Evaluation of Atypical Chemokine Receptor Expression in T Cell Subsets." Cells 11, no. 24 (2022): 4099. http://dx.doi.org/10.3390/cells11244099.

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Chemokines are molecules that pertain to a family of small cytokines and can generate cell chemotaxis through the interaction with their receptors. Chemokines can trigger signaling via conventional G-protein-coupled receptors or through atypical chemokine receptors. Currently, four atypical chemokine receptors have been are described (ACKR1, ACKR2, ACKR3 and ACKR4). ACKRs are expressed in various cells and tissues, including T lymphocytes. These receptors’ main function is related to the internalization and degradation of chemokines, as well as to the inflammation control. However, the express
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Miyabe, Yoshishige, Chie Miyabe, Vinidhra Mani, Thorsten R. Mempel, and Andrew D. Luster. "Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation." Science Immunology 4, no. 35 (2019): eaav5951. http://dx.doi.org/10.1126/sciimmunol.aav5951.

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Chemoattractant-induced arrest of circulating leukocytes and their subsequent diapedesis is a fundamental component of inflammation. However, how tissue-derived chemoattractants are transported into the blood vessel lumen to induce leukocyte entry into tissue is not well understood. Here, intravital microscopy in live mice has shown that the “atypical” complement C5a receptor 2 (C5aR2) and the atypical chemokine receptor 1 (ACKR1) expressed on endothelial cells were required for the transport of C5a and CXCR2 chemokine ligands, respectively, into the vessel lumen in a murine model of immune co
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Leick, Marion, Julie Catusse, and Meike Burger. "The Atypical Chemokine Receptor CRAM Mediates CCL19 Transcytosis through Endothelial Cells and Modulates CCL19 Activation of Non-Hodgkin Lymphoma B Cells." Blood 114, no. 22 (2009): 2672. http://dx.doi.org/10.1182/blood.v114.22.2672.2672.

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Abstract Abstract 2672 Poster Board II-648 Introduction: Chemokines work as cellular recruitment molecules. Specific combinations of chemokines, receptors, and adhesion molecules determine which subgroups of leukocytes migrate and what their destinations are. Chemokine receptor expression and activation on malignant cells may be involved in the growth, survival and migration of cancer cells as well as in the tumor vascularisation. CCR7, by binding the chemokines CCL19 and CCL21, is centrally involved in B cell localisation to the secondary lymphoid organs and therefore implicated in lymphadeno
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Dissertations / Theses on the topic "Atypical Chemokine Receptors"

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Tiplady, Eleanor Margaret. "Expression and modulation of atypical chemokine receptors on epithelial cells." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30618/.

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The immune system relies on the correct spatial and temporal positioning of cells in order to function; cells need to be able to move throughout the circulatory system to survey for pathogens, to migrate from their resident sites in tissues when they sense infection or injury to alert other cells, or to migrate to the site of damage or infection to help mobilise a response. These functions often involve chemokines, small cytokines that signal through chemokine receptors, which are G-protein coupled receptors expressed on the cell membrane. Different chemokines are regulated differentially and
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Benoit, Alice. "Identification du rôle de l’hypoxie dépendante de HIF-1α dans la régulation de l’expression de ACKR2 (Atypical Chemokine Receptor 2) dans le cancer". Electronic Thesis or Diss., Université de Lorraine, 2024. http://www.theses.fr/2024LORR0051.

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Les thérapies anti-cancéreuses, notamment l'immunothérapie, ont fait des progrès considérables ces dernières années ; cependant, seul un petit nombre de patients en tire un bénéfice clinique important et durable. Cela s'explique en partie par l'échec des cellules immunitaires cytotoxiques à infiltrer le microenvironnement des tumeurs. L'infiltration immunitaire dépend notamment du réseau de chimiokines, régulé en partie par les ACKRs. Le but de ce projet de thèse était d'étudier les mécanismes impliqués dans la régulation de ACKR2, qui est impliqué dans la régulation du réseau de chimiokines p
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Yu, Tian. "Role of atypical chemokine receptor-2 in ocular inflammation." Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=229021.

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The atypical chemokine receptor-2 (ACKR2) is a chemokine decoy receptor that recognises pro-inflammatory CC chemokines. Many studies showed up-regulated inflammation and delayed resolution of inflammatory responses in ACKR2-/- mice. Furthermore, in the absence of ACKR2, lymphatic endothelial cells (LEC) fail to regulate the expression of pro-inflammatory CC chemokines leading to the excessive peri-lymphatic accumulation of leukocytes. As a result, the migration of antigen presenting cells (APC) through lymphatic vessels may be impaired due to lymphatic congestion. In addition, ACKR2 was shown
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Hurson, Catherine Eileen. "Expression and function of the atypical chemokine receptor CCX-CKR." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2718/.

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The ability to clear infections and repair injury is dependent on the coordinated migration of immune cells, or leukocytes. These cells can directly destroy invading pathogens and also produce a variety of bioactive factors that promote pathogen clearance. Interactions between immune cells occur both at the site of inflammation and in specialised lymphoid organs throughout the body. The efficiency and specificity of these interactions relies on the production of a family of molecules called chemotactic cytokines, or chemokines, that drive leukocyte migration. Cells express specific profiles of
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King, Vicky. "Assessment of the therapeutic potential of the atypical chemokine receptor, D6." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/2165/.

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Infiltration of inflammatory cells into the tissue during the inflammatory response is beneficial to the host. Chemokines and their receptors are instrumental in this process by influencing the migration and behaviour of leukocytes in the tissue. However, prolonged inflammation is associated with many diseases. In recent years, a family of atypical receptors have emerged which do not seem to signal. One of these receptors, D6, is able to internalise and degrade 12 pro-inflammatory CC chemokines and has a role in the resolution of the inflammatory response. Here, using a murine transgenic appro
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Teoh, Pek Joo. "The role of the atypical chemokine receptor D6 in the placenta." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5098/.

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D6 is an atypical chemokine receptor related to CCR1-5 that binds to many inflammatory CC chemokines. Experiments using transfected cell lines have shown that upon binding to a chemokine ligand D6 does not trigger cellular signalling pathways, but rather acts to scavenge the bound ligand. It achieves this by constitutively travelling to and from the cell surface via early and recycling endosomes, internalising chemokines bound when it is at the cell surface. Over time, D6 removes a large amount of ligands from the extracellular compartment. In vivo, this scavenging activity is thought to regul
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Lucas, Beth. "Expression and function of the atypical chemokine receptor CCRL1 in the thymus." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5971/.

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Thymus colonisation and thymocyte positioning are mediated by interactions involving CCR7 and CCR9 and their respective ligands CCL19/CCL21 and CCL25. These chemokines also interact with the atypical receptor CCRL1, which is expressed in the thymus and has recently been reported to play an important role in normal abT-cell development. Our study has mapped CCRL1 expression within the adult and embryonic thymus, and shows that CCRL1 is expressed within the thymic cortex, at the subcapsular zone, and surrounding vessels at the corticomedullary junction. We have used flow cytometry to show CCRL1
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Vacchini, A. "ANALYSIS OF BIASED SIGNALING IN THE CHEMOKINE SYSTEM." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/365864.

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Chemokines constitute a family of almost 50 small secreted cytokines, recognized by about 20 different 7TM spanning G protein coupled receptors (GPCRs), that activating pertussis toxin sensitive G proteins induce cell migration. These receptor are abundantly expressed by leukocytes and, controlling cell migration, they dictate leukocyte positioning during homeostatic patrolling within peripheral tissues, their maintenance in bone marrow during maturation and in addition mediate their recruitment to inflamed tissues. Upon inflammation in fact a number of chemokines are produced or activated by
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Shams, Kave. "The role and regulation of the atypical chemokine receptor 2 in psoriasiform inflammation." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8121/.

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Psoriasis is a common, debilitating systemic inflammatory disorder that is characterised by sharply demarcated, thick, erythematous scaly skin plaques. Such plaques commonly appear on skin that is subjected to repeated tensile trauma, such as elbows, knees and flexures. The mechanism by which these inflammatory lesions are spatially restricted is not known and yet knowledge of this could be of critical importance for our understanding of this disease. Chemokines are the principal regulators of leukocyte migration and play a critical role in the initiation and maintenance of inflammation. The a
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Korniejewska, Anna. "Characterisation of the chemokine receptor CXCR3 and its atypical variants in human T lymphocytes." Thesis, University of Bath, 2009. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518106.

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The chemokine receptor CXCR3 and its agonists CXCL9/Mig, CXCL10/IP-10 and CXCL11/I-TAC are involved in a variety of inflammatory disorders including multiple sclerosis, rheumatoid arthritis, psoriasis and sarcoidosis. CXCL11 has also been reported to bind to an additional receptor, namely CXCR7, which also interacts with CXCL12. Two alternatively spliced variants of the human CXCR3 receptor have been described, namely CXCR3-B and CXCR3-alt. The human CXCR3-B has been found to bind CXCL9, CXCL10, CXCL11 as well as an additional agonist CXCL4/PF4. In contrast, CXCR3-alt only binds CXCL11. This w
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Books on the topic "Atypical Chemokine Receptors"

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Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease
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Book chapters on the topic "Atypical Chemokine Receptors"

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Singh, Mark D., Robert J. B. Nibbs, and Gerard J. Graham. "The Atypical Chemokine Receptors." In Methods and Principles in Medicinal Chemistry. Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527631995.ch4.

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Bonecchi, Raffaella, Matteo Massara, and Massimo Locati. "Atypical Chemokine Receptors." In Encyclopedia of Immunobiology. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-374279-7.10009-8.

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Bonecchi, Raffaella, Annalisa Del Prete, and Silvano Sozzani. "Atypical Chemokine Receptors." In Reference Module in Life Sciences. Elsevier, 2024. https://doi.org/10.1016/b978-0-12-824465-4.00138-1.

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Werth, Kathrin, and Reinhold Förster. "Active Shaping of Chemokine Gradients by Atypical Chemokine Receptors." In Methods in Enzymology. Elsevier, 2016. http://dx.doi.org/10.1016/bs.mie.2015.09.008.

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Borroni, Elena, Cinzia Cancellieri, Massimo Locati, and Raffaella Bonecchi. "Dissecting Trafficking and Signaling of Atypical Chemokine Receptors." In Methods in Enzymology. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-391862-8.00008-9.

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Lokeshwar, Bal L., Georgios Kallifatidis, and James J. Hoy. "Atypical chemokine receptors in tumor cell growth and metastasis." In Advances in Cancer Research. Elsevier, 2020. http://dx.doi.org/10.1016/bs.acr.2019.12.002.

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Luís, Rafael, Giulia D’Uonnolo, Christie B. Palmer, et al. "Nanoluciferase-based methods to monitor activation, modulation and trafficking of atypical chemokine receptors." In Methods in Cell Biology. Elsevier, 2022. http://dx.doi.org/10.1016/bs.mcb.2022.03.002.

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Sjöberg, Elin, Max Meyrath, Andy Chevigné, Arne Östman, Martin Augsten, and Martyna Szpakowska. "The diverse and complex roles of atypical chemokine receptors in cancer: From molecular biology to clinical relevance and therapy." In Advances in Cancer Research. Elsevier, 2020. http://dx.doi.org/10.1016/bs.acr.2019.12.001.

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Kleist, Andrew B., Francis Peterson, Robert C. Tyler, Martin Gustavsson, Tracy M. Handel, and Brian F. Volkman. "Solution NMR spectroscopy of GPCRs: Residue-specific labeling strategies with a focus on 13C-methyl methionine labeling of the atypical chemokine receptor ACKR3." In Methods in Cell Biology. Elsevier, 2019. http://dx.doi.org/10.1016/bs.mcb.2018.09.004.

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Conference papers on the topic "Atypical Chemokine Receptors"

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Jenkins, Brittany D., Rupali Hire, Elizabeth Howerth, Michele Monteil, Rachel Martini, and Melissa B. Davis. "Abstract 953: Atypical chemokine receptor 1 (ACKR1/DARC) expressing tumors are associated with distinct recruitment of immune cells and increased pro-inflammatory chemokines." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-953.

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Jenkins, Brittany D., Rachel N. Martini, Rupali Hire, Michele A. Monteil, and Melissa B. Davis. "Abstract B39: Distinct recruitment of tumor-associated immune cells correlates with increased pro-malignant chemokines in tumors expressing epithelial Atypical Chemokine Receptor 1 (ACKR1/DARC)." In Abstracts: Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 25-28, 2016; Fort Lauderdale, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7755.disp16-b39.

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Salazar, Nicole, Daniel Muñoz, and Bal L. Lokeshwar. "Abstract C210: Atypical chemokine receptor 3/CXCR7 and EGFR interact to control breast cancer growth." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-c210.

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Jenkins, Brittany D., Rachel N. Martini, Inasia Brown, and Melissa B. Davis. "Abstract 5071: The functional relevance of Atypical Chemokine Receptor 1 (ACKR1/DARC) genetic isoforms in breast cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5071.

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Jenkins, Brittany D., Rachel Martini, Kevin Gardner, et al. "Abstract 4565: The functional role of atypical chemokine receptor 1 in immune cell regulation of breast cancer." 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.sabcs18-4565.

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Jenkins, Brittany D., Rachel Martini, Kevin Gardner, et al. "Abstract 4565: The functional role of atypical chemokine receptor 1 in immune cell regulation of breast cancer." 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.am2019-4565.

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Kim, Nayoung, Seung-Woo Baek, Hyewon Ryu, et al. "Abstract 3947: Atypical chemokine receptor ACKR3 expression is associated with aggressive behavior and poor prognosis in gastric cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3947.

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Jenkins, BD, RN Martini, R. Hire, MA Monteil, and MB Davis. "Abstract P6-01-11: Distinct recruitment of tumor-associated immune cells correlates with increased pro-malignant chemokines in tumors expressing epithelial atypical chemokine receptor 1 (ACKR1/DARC), indicating a unique tumor microenvironment." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p6-01-11.

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