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Journal articles on the topic 'Atypical Chemokine Receptors'

Author: Grafiati

Published: 2 November 2024

Last updated: 31 July 2025

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1

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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Chevigné, Andy, Bassam Janji, Max Meyrath, et al. "CXCL10 Is an Agonist of the CC Family Chemokine Scavenger Receptor ACKR2/D6." Cancers 13, no. 5 (2021): 1054. http://dx.doi.org/10.3390/cancers13051054.

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Atypical chemokine receptors (ACKRs) are important regulators of chemokine functions. Among them, the atypical chemokine receptor ACKR2 (also known as D6) has long been considered as a scavenger of inflammatory chemokines exclusively from the CC family. In this study, by using highly sensitive β-arrestin recruitment assays based on NanoBiT and NanoBRET technologies, we identified the inflammatory CXC chemokine CXCL10 as a new strong agonist ligand for ACKR2. CXCL10 is known to play an important role in the infiltration of immune cells into the tumour bed and was previously reported to bind to

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Samus, Maryna, and Antal Rot. "Atypical chemokine receptors in cancer." Cytokine 176 (April 2024): 156504. http://dx.doi.org/10.1016/j.cyto.2024.156504.

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Blanchet, Xavier, Christian Weber, and Philipp von Hundelshausen. "Chemokine Heteromers and Their Impact on Cellular Function—A Conceptual Framework." International Journal of Molecular Sciences 24, no. 13 (2023): 10925. http://dx.doi.org/10.3390/ijms241310925.

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Chemoattractant cytokines or chemokines are proteins involved in numerous biological activities. Their essential role consists of the formation of gradient and (immune) cell recruitment. Chemokine biology and its related signaling system is more complex than simple ligand–receptor interactions. Beside interactions with their cognate and/or atypical chemokine receptors, and glycosaminoglycans (GAGs), chemokines form complexes with themselves as homo-oligomers, heteromers and also with other soluble effector proteins, including the atypical chemokine MIF, carbohydrate-binding proteins (galectins

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Borroni, Elena M., Cinzia Cancellieri, Alessandro Vacchini та ін. "β-Arrestin–Dependent Activation of the Cofilin Pathway Is Required for the Scavenging Activity of the Atypical Chemokine Receptor D6". Science Signaling 6, № 273 (2013): ra30. http://dx.doi.org/10.1126/scisignal.2003627.

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Chemokines promote the recruitment of leukocytes to sites of infection and inflammation by activating conventional heterotrimeric guanine nucleotide–binding protein (G protein)–coupled receptors (GPCRs). Chemokines are also recognized by a set of atypical chemokine receptors (ACRs), which cannot induce directional cell migration but are required for the generation of chemokine gradients in tissues. ACRs are presently considered “silent receptors” because no G protein–dependent signaling activity is observed after their engagement by cognate ligands. We report that engagement of the ACR D6 by i

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Schlecht-Louf, Géraldine, Claire Deback, and Françoise Bachelerie. "The Chemokine System in Oncogenic Pathways Driven by Viruses: Perspectives for Cancer Immunotherapy." Cancers 14, no. 3 (2022): 848. http://dx.doi.org/10.3390/cancers14030848.

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Chemokines interact with glycosaminoglycans of the extracellular matrix and activate heptahelical cellular receptors that mainly consist of G Protein-Coupled Receptors and a few atypical receptors also with decoy activity. They are well-described targets of oncogenic pathways and key players in cancer development, invasiveness, and metastasis acting both at the level of cancer cells and cells of the tumor microenvironment. Hence, they can regulate cancer cell proliferation and survival and promote immune or endothelial cell migration into the tumor microenvironment. Additionally, oncogenic vir

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Melgrati, Serena, Egle Radice, Rafet Ameti, et al. "Atlas of the anatomical localization of atypical chemokine receptors in healthy mice." PLOS Biology 21, no. 5 (2023): e3002111. http://dx.doi.org/10.1371/journal.pbio.3002111.

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Atypical chemokine receptors (ACKRs) scavenge chemokines and can contribute to gradient formation by binding, internalizing, and delivering chemokines for lysosomal degradation. ACKRs do not couple to G-proteins and fail to induce typical signaling induced by chemokine receptors. ACKR3, which binds and scavenges CXCL12 and CXCL11, is known to be expressed in vascular endothelium, where it has immediate access to circulating chemokines. ACKR4, which binds and scavenges CCL19, CCL20, CCL21, CCL22, and CCL25, has also been detected in lymphatic and blood vessels of secondary lymphoid organs, wher

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Purvanov, Vladimir, Christoph Matti, Guerric P. B. Samson, Ilona Kindinger, and Daniel F. Legler. "Fluorescently Tagged CCL19 and CCL21 to Monitor CCR7 and ACKR4 Functions." International Journal of Molecular Sciences 19, no. 12 (2018): 3876. http://dx.doi.org/10.3390/ijms19123876.

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Chemokines are essential guidance cues orchestrating cell migration in health and disease. Cognate chemokine receptors sense chemokine gradients over short distances to coordinate directional cell locomotion. The chemokines CCL19 and CCL21 are essential for recruiting CCR7-expressing dendritic cells bearing pathogen-derived antigens and lymphocytes to lymph nodes, where the two cell types meet to launch an adaptive immune response against the invading pathogen. CCR7-expressing cancer cells are also recruited by CCL19 and CCL21 to metastasize in lymphoid organs. In contrast, atypical chemokine

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Patel, Manish, Iain McInnes, and Gerard Graham. "Atypical Chemokine Receptors in Inflammatory Disease." Current Molecular Medicine 9, no. 1 (2009): 86–93. http://dx.doi.org/10.2174/156652409787314480.

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Segerer, Stephan, Jan Jedlicka, and Rudolf P. Wüthrich. "Atypical Chemokine Receptors in Renal Inflammation." Nephron Experimental Nephrology 115, no. 4 (2010): e89-e95. http://dx.doi.org/10.1159/000313489.

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Bachelerie, Françoise, Gerard J. Graham, Massimo Locati, et al. "New nomenclature for atypical chemokine receptors." Nature Immunology 15, no. 3 (2014): 207–8. http://dx.doi.org/10.1038/ni.2812.

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21

Nibbs, Robert J. B., and Gerard J. Graham. "Immune regulation by atypical chemokine receptors." Nature Reviews Immunology 13, no. 11 (2013): 815–29. http://dx.doi.org/10.1038/nri3544.

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Cancellieri, Cinzia, Alessandro Vacchini, Massimo Locati, Raffaella Bonecchi, and Elena M. Borroni. "Atypical chemokine receptors: from silence to sound." Biochemical Society Transactions 41, no. 1 (2013): 231–36. http://dx.doi.org/10.1042/bst20120246.

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ACRs (atypical chemokine receptors) were initially referred to as ‘silent’ receptors on the basis of a lack of signalling and functional activities that are typically observed with conventional chemokine receptors. Although ACRs do not directly induce cell migration, they indirectly control leucocyte recruitment by shaping chemokine gradients in tissues through degradation, transcytosis or local concentration of their cognate ligands. Recent evidence also suggests that these biological activities are supported by G-protein-independent, β-arrestin-dependent signalling events. In the present art

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Tsou, Chia-Lin, Ron P. Gladue, Laurie A. Carroll, et al. "Identification of C-C Chemokine Receptor 1 (CCR1) as the Monocyte Hemofiltrate C-C Chemokine (HCC)-1 Receptor." Journal of Experimental Medicine 188, no. 3 (1998): 603–8. http://dx.doi.org/10.1084/jem.188.3.603.

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Hemofiltrate C-C chemokine (HCC)-1 is a recently cloned C-C chemokine that is structurally similar to macrophage inflammatory protein (MIP)-1α. Unlike most chemokines, it is constitutively secreted by tissues and is present at high concentrations in normal human plasma. Also atypical for chemokines, HCC-1 is reported not to be chemotactic for leukocytes. In this paper, we have investigated the chemokine receptor usage and downstream signaling pathways of HCC-1. Cross-desensitization experiments using THP-1 cells suggested that HCC-1 and MIP-1α activated the same receptor. Experiments using a p

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Mackie, Duncan I., Natalie R. Nielsen, Matthew Harris, et al. "RAMP3 determines rapid recycling of atypical chemokine receptor-3 for guided angiogenesis." Proceedings of the National Academy of Sciences 116, no. 48 (2019): 24093–99. http://dx.doi.org/10.1073/pnas.1905561116.

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Receptor-activity–modifying proteins (RAMPs) are single transmembrane-spanning proteins which serve as molecular chaperones and allosteric modulators of G-protein–coupled receptors (GPCRs) and their signaling pathways. Although RAMPs have been previously studied in the context of their effects on Family B GPCRs, the coevolution of RAMPs with many GPCR families suggests an expanded repertoire of potential interactions. Using bioluminescence resonance energy transfer-based and cell-surface expression approaches, we comprehensively screen for RAMP interactions within the chemokine receptor family

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Khare, Tripti, Marc Bissonnette, and Sharad Khare. "CXCL12-CXCR4/CXCR7 Axis in Colorectal Cancer: Therapeutic Target in Preclinical and Clinical Studies." International Journal of Molecular Sciences 22, no. 14 (2021): 7371. http://dx.doi.org/10.3390/ijms22147371.

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Chemokines are chemotactic cytokines that promote cancer growth, metastasis, and regulate resistance to chemotherapy. Stromal cell-derived factor 1 (SDF1) also known as C-X-C motif chemokine 12 (CXCL12), a prognostic factor, is an extracellular homeostatic chemokine that is the natural ligand for chemokine receptors C-X-C chemokine receptor type 4 (CXCR4), also known as fusin or cluster of differentiation 184 (CD184) and chemokine receptor type 7 (CXCR7). CXCR4 is the most widely expressed rhodopsin-like G protein coupled chemokine receptor (GPCR). The CXCL12–CXCR4 axis is involved in tumor gr

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Lindsay, Hunter G., Colby J. Hendrix, Josue D. Gonzalez Murcia, Christopher Haynie, and K. Scott Weber. "The Role of Atypical Chemokine Receptors in Neuroinflammation and Neurodegenerative Disorders." International Journal of Molecular Sciences 24, no. 22 (2023): 16493. http://dx.doi.org/10.3390/ijms242216493.

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Neuroinflammation is associated with several neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). Neuroinflammation provides protection in acute situations but results in significant damage to the nervous system if chronic. Overexpression of chemokines within the brain results in the recruitment and activation of glial and peripheral immune cells which can propagate a cascading inflammatory response, resulting in neurodegeneration and the onset of neurodegenerative disorders. Recent work has identified the role of atypical chem

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Dragan, Paulina, Matthew Merski, Szymon Wiśniewski, Swapnil Ganesh Sanmukh, and Dorota Latek. "Chemokine Receptors—Structure-Based Virtual Screening Assisted by Machine Learning." Pharmaceutics 15, no. 2 (2023): 516. http://dx.doi.org/10.3390/pharmaceutics15020516.

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Chemokines modulate the immune response by regulating the migration of immune cells. They are also known to participate in such processes as cell–cell adhesion, allograft rejection, and angiogenesis. Chemokines interact with two different subfamilies of G protein-coupled receptors: conventional chemokine receptors and atypical chemokine receptors. Here, we focused on the former one which has been linked to many inflammatory diseases, including: multiple sclerosis, asthma, nephritis, and rheumatoid arthritis. Available crystal and cryo-EM structures and homology models of six chemokine receptor

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Eller, Kathrin, and Alexander R. Rosenkranz. "Atypical chemokine receptors—“chemokine PACMANs” as new therapeutic targets in glomerulonephritis." Kidney International 93, no. 4 (2018): 774–75. http://dx.doi.org/10.1016/j.kint.2017.12.021.

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Bryce, Steven, Andrew Luster, Gerry Graham, and Rob Nibbs. "The ‘atypical’ chemokine receptor CCRL1 aids dendritic cell migration from inflamed skin. (P6352)." Journal of Immunology 190, no. 1_Supplement (2013): 199.2. http://dx.doi.org/10.4049/jimmunol.190.supp.199.2.

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Abstract Chemokine-directed leukocyte migration is essential for immune and inflammatory responses. The chemokine receptor CCR7, by responding to chemokines CCL19 and CCL21, is critical in regulating the recruitment of dendritic cells (DC), from peripheral tissues to draining lymph nodes (LNs). CCR7 is required for DC entry into lymphatic vessels, and for the passage of these cells across subcapsular sinus of the lymph node. Here, they initiate adaptive immune responses by priming antigen-specific T cells. CCRL1, an unexpected second receptor for CCL19 and CCL21, belongs to the family of atypi

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Massara, Matteo, Ornella Bonavita, Alberto Mantovani, Massimo Locati, and Raffaella Bonecchi. "Atypical chemokine receptors in cancer: friends or foes?" Journal of Leukocyte Biology 99, no. 6 (2016): 927–33. http://dx.doi.org/10.1189/jlb.3mr0915-431rr.

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Le Mercier, Alan, Remy Bonnavion, Weijia Yu, et al. "GPR182 is an endothelium-specific atypical chemokine receptor that maintains hematopoietic stem cell homeostasis." Proceedings of the National Academy of Sciences 118, no. 17 (2021): e2021596118. http://dx.doi.org/10.1073/pnas.2021596118.

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G protein–coupled receptor 182 (GPR182) has been shown to be expressed in endothelial cells; however, its ligand and physiological role has remained elusive. We found GPR182 to be expressed in microvascular and lymphatic endothelial cells of most organs and to bind with nanomolar affinity the chemokines CXCL10, CXCL12, and CXCL13. In contrast to conventional chemokine receptors, binding of chemokines to GPR182 did not induce typical downstream signaling processes, including Gq- and Gi-mediated signaling or β-arrestin recruitment. GPR182 showed relatively high constitutive activity in regard to

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Martini, Rachel, Petros Nikolinakos, Jamie Hodgson, Brittany Jenkins, and Melissa Davis. "The role of atypical chemokine receptor-1 in breast cancer immune response." Journal of Clinical Oncology 35, no. 15_suppl (2017): e23072-e23072. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e23072.

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e23072 Background: Interactions between chemokines and their receptors can regulate anti-tumor response by influencing the migration of immune cells. Atypical Chemokine Receptor 1 (ACKR1/DARC), a genetically diverse transmembrane GPCR, acts as a decoy receptor for a variety of CXC and CC chemokines, including those with pro-malignant and pro-inflammatory effects, such as CCL2 and CXCL8 . The purpose of this study is to determine if the migration of tumor-associated immune cells is unique based on epithelial ACKR1 expression on breast cancer cells, and if this association is correlated to an in

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Graham, G. J., M. Locati, A. Mantovani, A. Rot, and M. Thelen. "The biochemistry and biology of the atypical chemokine receptors." Immunology Letters 145, no. 1-2 (2012): 30–38. http://dx.doi.org/10.1016/j.imlet.2012.04.004.

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Majumdar, Shamik, Sergio M. Pontejo, Joseph Weaver, and Philip M. Murphy. "Ackr1-deficient mice are protected from lethal SARS-CoV-2 challenge." Journal of Immunology 210, no. 1_Supplement (2023): 79.08. http://dx.doi.org/10.4049/jimmunol.210.supp.79.08.

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Abstract To date, there have been more than 613 million confirmed cases of COVID-19, with over 6 million deaths worldwide. In severe cases, the causative agent of the COVID-19, SARS-CoV-2, induces acute respiratory distress syndrome. To study the roles of chemokine pathways during COVID-19 pathogenesis, we performed an infection screen in mice deficient in chemokine ligands and receptors using the mouse-adapted strain of the virus. Weight loss and death were recorded for 2 weeks after infection of wild type mice, and mice genetically deficient for Ccr2, Ccr5, Ccr6, Cxcr3, Cxcr6, Cxcl10 or the

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Johnsson, H., J. Cole, G. Wilson, et al. "SAT0351 CHEMOKINE PATHWAYS ARE ENRICHED IN PSORIATIC ARTHRITIS (PSA) SKIN LESIONS WITH INCREASED EXPRESSION OF ATYPICAL CHEMOKINE RECEPTOR 2 (ACKR2)." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 1121.2–1122. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2980.

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Background:Skin in people with psoriasis has been comprehensively studied; uninvolved skin has abnormal gene expression. Less is known specifically about skin in PsA, the assumption being that it is identical to psoriasis. Chemokines and ACKR2 are among the upregulated genes in uninvolved psoriasis compared to healthy skin[1]. ACKR2 is a scavenging receptor of inflammatory CC chemokines and has been proposed as a regulator of cutaneous inflammation in psoriasis. It has not been studied in PsA.Objectives:To compare the transcriptome of PsA lesional, PsA uninvolved and healthy control skin and e

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Russo, Remo C., Benedetta Savino, Massimiliano Mirolo та ін. "The atypical chemokine receptor ACKR2 drives pulmonary fibrosis by tuning influx of CCR2+ and CCR5+ IFNγ-producing γδT cells in mice". American Journal of Physiology-Lung Cellular and Molecular Physiology 314, № 6 (2018): L1010—L1025. http://dx.doi.org/10.1152/ajplung.00233.2017.

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Chemokines coordinate lung inflammation and fibrosis by acting on chemokine receptors expressed on leukocytes and other cell types. Atypical chemokine receptors (ACKRs) bind, internalize, and degrade chemokines, tuning homeostasis and immune responses. ACKR2 recognizes and decreases the levels of inflammatory CC chemokines. The role of ACKR2 in fibrogenesis is unknown. The purpose of the study was to investigate the role of ACKR2 in the context of pulmonary fibrosis. The effects of ACKR2 expression and deficiency during inflammation and fibrosis were analyzed using a bleomycin-model of fibrosi

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Di Donato, Rachele, Raffaella Bonecchi, and Francesca Albano. "Canonical and atypical chemokine receptors in the neutrophil life cycle." Cytokine 169 (September 2023): 156297. http://dx.doi.org/10.1016/j.cyto.2023.156297.

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Sinitski, Dzmitry, Christos Kontos, Christine Krammer, Yaw Asare, Aphrodite Kapurniotu, and Jürgen Bernhagen. "Macrophage Migration Inhibitory Factor (MIF)-Based Therapeutic Concepts in Atherosclerosis and Inflammation." Thrombosis and Haemostasis 119, no. 04 (2019): 553–66. http://dx.doi.org/10.1055/s-0039-1677803.

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AbstractChemokines orchestrate leukocyte recruitment in atherosclerosis and their blockade is a promising anti-atherosclerotic strategy, but few chemokine-based approaches have advanced into clinical trials, in part owing to the complexity and redundancy of the chemokine network. Macrophage migration inhibitory factor (MIF) is a pivotal mediator of atherosclerotic lesion formation. It has been characterized as an inflammatory cytokine and atypical chemokine that promotes atherogenic leukocyte recruitment and lesional inflammation through interactions with the chemokine receptors CXCR2 and CXCR

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Cheng, Xiaoyun, and Mien-Chie Hung. "Regulation of Breast Cancer Metastasis by Atypical Chemokine Receptors: Fig. 1." Clinical Cancer Research 15, no. 9 (2009): 2951–53. http://dx.doi.org/10.1158/1078-0432.ccr-09-0141.

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Degroot, Gaetan-Nagim, Valentin Lepage, Marc Parmentier та Jean-Yves Springael. "The Atypical Chemerin Receptor GPR1 Displays Different Modes of Interaction with β-Arrestins in Humans and Mice with Important Consequences on Subcellular Localization and Trafficking". Cells 11, № 6 (2022): 1037. http://dx.doi.org/10.3390/cells11061037.

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Atypical chemokine receptors (ACKRs) have emerged as a subfamily of chemokine receptors regulating the local bioavailability of their ligands through scavenging, concentration, or transport. The biological roles of ACKRs in human physiology and diseases are often studied by using transgenic mouse models. However, it is unknown whether mouse and human ACKRs share the same properties. In this study, we compared the properties of the human and mouse atypical chemerin receptor GPR1 and showed that they behave differently regarding their interaction with β-arrestins. Human hGPR1 interacts with β-ar

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Tan, Wee Yee, Boon Yin Khoo, and Ai Lan Chew. "Pichia-Expressed Recombinant D6 and DARC Negatively Affect Cell Migration and Invasion of Breast Cancer Cells." Sains Malaysiana 50, no. 10 (2021): 3015–33. http://dx.doi.org/10.17576/jsm-2021-5010-15.

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Atypical chemokine receptor proteins are termed ‘decoy proteins’ as their binding to the respective ligands does not lead to a typical signaling pathway but intercepts the action of chemokines. This method of chemokine activity regulation may also function in tumor suppression. D6 and DARC (Duffy Antigen Receptor for Chemokines) have been reported as decoy chemokine receptors in cancer studies. Purified Pichia-expressed D6 and DARC, produced in-house, were used in cell-based studies to test their biological activities. Cell viability tests showed that recombinant D6 and DARC did not affect cel

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Pan, Li, Jianliang Lv, Zhongwang Zhang, and Yongguang Zhang. "Adaptation and Constraint in the Atypical Chemokine Receptor Family in Mammals." BioMed Research International 2018 (September 24, 2018): 1–9. http://dx.doi.org/10.1155/2018/9065181.

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Atypical chemokine receptors (ACKRs) are a subclass of G protein-coupled receptors characterized by promiscuity of ligand binding and an obvious inability to signal after ligand binding. Although some discoveries regarding this family in Homo sapiens and other species have been reported in some studies, the evolution and function of multiple ACKR in mammals have not yet been clearly understood. We performed an evolutionary analysis of ACKR genes (ACKR1, ACKR2, ACKR3, and ACKR4) in mammals. Ninety-two full-length ACKR genes from 27 mammal species were retrieved from the Genbank and Ensemble dat

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Burger, Nathalie, Andrea Haerzschel, Marion Leick, Tanja Nicole Hartmann, Julie Catusse, and Meike Burger. "CCL19 Induced Responses Are Differentially Regulated by Atypical Chemokine Receptor CRAM and Its Classical Chemokine Receptor CCR7 in B-CLL Cells." Blood 118, no. 21 (2011): 4896. http://dx.doi.org/10.1182/blood.v118.21.4896.4896.

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Abstract Abstract 4896 Introduction: Chemokines are known to play an important role in the migration and survival of B-CLL cells. The non-signalling chemokine receptors, including DARC, D6 and CCX-CKR, have recently been shown to be involved in chemokine clearance and activity regulation. The human chemokine receptor CRAM is the most recently identified member of this atypical group. CRAM is expressed on B cells in a maturation-stage dependent manner, and to variable degrees on B-CLL cells. We have recently shown that it competitively binds CCL19 and that this binding is not followed by classi

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Ford, Laura B., Vuk Cerovic, Simon W. F. Milling, Gerard J. Graham, Chris A. H. Hansell, and Robert J. B. Nibbs. "Characterization of Conventional and Atypical Receptors for the Chemokine CCL2 on Mouse Leukocytes." Journal of Immunology 193, no. 1 (2014): 400–411. http://dx.doi.org/10.4049/jimmunol.1303236.

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Calvello, Rosa, Chiara Porro, Dario Domenico Lofrumento, Melania Ruggiero, Maria Antonietta Panaro, and Antonia Cianciulli. "Decoy Receptors Regulation by Resveratrol in Lipopolysaccharide-Activated Microglia." Cells 12, no. 5 (2023): 681. http://dx.doi.org/10.3390/cells12050681.

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Resveratrol is a polyphenol that acts as antioxidants do, protecting the body against diseases, such as diabetes, cancer, heart disease, and neurodegenerative disorders, such as Alzheimer’s (AD) and Parkinson’s diseases (PD). In the present study, we report that the treatment of activated microglia with resveratrol after prolonged exposure to lipopolysaccharide is not only able to modulate pro-inflammatory responses, but it also up-regulates the expression of decoy receptors, IL-1R2 and ACKR2 (atypical chemokine receptors), also known as negative regulatory receptors, which are able to reduce

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Kleist, Andrew B., Shawn Jenjak, Andrija Sente та ін. "Conformational selection guides β-arrestin recruitment at a biased G protein–coupled receptor". Science 377, № 6602 (2022): 222–28. http://dx.doi.org/10.1126/science.abj4922.

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G protein–coupled receptors (GPCRs) recruit β-arrestins to coordinate diverse cellular processes, but the structural dynamics driving this process are poorly understood. Atypical chemokine receptors (ACKRs) are intrinsically biased GPCRs that engage β-arrestins but not G proteins, making them a model system for investigating the structural basis of β-arrestin recruitment. Here, we performed nuclear magnetic resonance (NMR) experiments on 13 CH 3 -ε–methionine–labeled ACKR3, revealing that β-arrestin recruitment is associated with conformational exchange at key regions of the extracellular liga

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Dobroch, Jakub, Klaudia Bojczuk, Adrian Kołakowski, Marta Baczewska, and Paweł Knapp. "The Exploration of Chemokines Importance in the Pathogenesis and Development of Endometrial Cancer." Molecules 27, no. 7 (2022): 2041. http://dx.doi.org/10.3390/molecules27072041.

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Endometrial cancer (EC) is one of the most frequent female malignancies. Because of a characteristic symptom, vaginal bleeding, EC is often diagnosed in an early stage. Despite that, some EC cases present an atypical course with rapid progression and poor prognosis. There have been multiple studies conducted on molecular profiling of EC in order to improve diagnostics and introduce personalized treatment. Chemokines—a protein family that contributes to inflammatory processes that may promote carcinogenesis—constitute an area of interest. Some chemokines and their receptors present alterations

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del Molino del Barrio, Irene, Georgina Wilkins, Annette Meeson, Simi Ali, and John Kirby. "Breast Cancer: An Examination of the Potential of ACKR3 to Modify the Response of CXCR4 to CXCL12." International Journal of Molecular Sciences 19, no. 11 (2018): 3592. http://dx.doi.org/10.3390/ijms19113592.

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Upon binding with the chemokine CXCL12, the chemokine receptor CXCR4 has been shown to promote breast cancer progression. This process, however, can be affected by the expression of the atypical chemokine receptor ACKR3. Given ACKR3’s ability to form heterodimers with CXCR4, we investigated how dual expression of both receptors differed from their lone expression in terms of their signalling pathways. We created single and double CXCR4 and/or ACKR3 Chinese hamster ovary (CHO) cell transfectants. ERK and Akt phosphorylation after CXCL12 stimulation was assessed and correlated with receptor inte

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Bachelerie, Francoise, Adit Ben-Baruch, Amanda M. Burkhardt, et al. "International Union of Basic and Clinical Pharmacology. LXXXIX. Update on the Extended Family of Chemokine Receptors and Introducing a New Nomenclature for Atypical Chemokine Receptors." Pharmacological Reviews 66, no. 1 (2013): 1–79. http://dx.doi.org/10.1124/pr.113.007724.

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Korbecki, Jan, Mateusz Bosiacki, Piotr Stasiak та ін. "Clinical Aspects and Significance of β-Chemokines, γ-Chemokines, and δ-Chemokines in Molecular Cancer Processes in Acute Myeloid Leukemia (AML) and Myelodysplastic Neoplasms (MDS)". Cancers 16, № 19 (2024): 3246. http://dx.doi.org/10.3390/cancers16193246.

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Background/Objectives: Acute myeloid leukemia (AML) is a type of leukemia with a very poor prognosis. Consequently, this neoplasm is extensively researched to discover new therapeutic strategies. One area of investigation is the study of intracellular communication and the impact of the bone marrow microenvironment on AML cells, with chemokines being a key focus. The roles of β-chemokines, γ-chemokines, and δ-chemokines in AML processes have not yet been sufficiently characterized. Methods: This publication summarizes all available knowledge about these chemotactic cytokines in AML and myelody

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