Relevant bibliographies by topics / Chemokine receptor

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Chemokine receptor'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Chemokine receptor"

1

Zhang, Peng-Fei, Chuang Wang, Le Zhang, and Qiu Li. "Reversing chemokine/chemokine receptor mismatch to enhance the antitumor efficacy of CAR-T cells." Immunotherapy 14, no. 6 (April 2022): 459–73. http://dx.doi.org/10.2217/imt-2021-0228.

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Currently, the antitumor efficacy of chimeric antigen receptor T cells in solid tumors is modest. Both chemokines and their receptors play a key role in the proliferation of cancer cells, tumor angiogenesis, organ-selective metastasis and migration of immune cells to solid tumors. Unfortunately, frequent chemokine/chemokine receptor ‘mismatch’ between effector cells and the tumor microenvironment results in inefficient T-cell infiltration and antitumor efficacy. Thus, reversing the ‘mismatch’ of chemokines and chemokine receptors appears to be a promising method for promoting T-cell infiltration into the tumor and enhancing their antitumor efficacy. In this review, we discuss functions of the chemokine/chemokine receptor axis in cancer immunity and the current understanding, challenges and prospects for improving the effect of chimeric antigen receptor T cells by reversing the mismatch between chemokines and 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 (October 25, 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 binding. Instead, these ‘atypical’ chemokine receptors are biochemically specialized for chemokine sequestration, acting to regulate chemokine bioavailability and thereby influence responses through signalling-competent chemokine receptors. This is of critical importance in vivo, as mice lacking D6 show exaggerated cutaneous inflammatory responses and an increased susceptibility to the development of skin cancer. CCX-CKR, on the other hand, is predicted to modulate homoeostatic lymphocyte and dendritic cell trafficking, key migratory events in acquired immune responses that are directed by CCX-CKR-binding chemokines. Thus studies on ‘atypical’ chemokine receptors are revealing functional and biochemical diversity within the chemokine receptor family and providing insights into novel mechanisms of chemokine regulation.
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Palacios-Arreola, M. Isabel, Karen E. Nava-Castro, Julieta I. Castro, Eduardo García-Zepeda, Julio C. Carrero, and Jorge Morales-Montor. "The Role of Chemokines in Breast Cancer Pathology and Its Possible Use as Therapeutic Targets." Journal of Immunology Research 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/849720.

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Chemokines are small proteins that primarily regulate the traffic of leukocytes under homeostatic conditions and during specific immune responses. The chemokine-chemokine receptor system comprises almost 50 chemokines and approximately 20 chemokine receptors; thus, there is no unique ligand for each receptor and the binding of different chemokines to the same receptor might have disparate effects. Complicating the system further, these effects depend on the cellular milieu. In cancer, although chemokines are associated primarily with the generation of a protumoral microenvironment and organ-directed metastasis, they also mediate other phenomena related to disease progression, such as angiogenesis and even chemoresistance. Therefore, the chemokine system is becoming a target in cancer therapeutics. We review the emerging data and correlations between chemokines/chemokine receptors and breast cancer, their implications in cancer progression, and possible therapeutic strategies that exploit the chemokine system.
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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 (September 10, 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 dissociation kinetic measurements coupled to β-arrestin recruitment assays to investigate ACKR3:chemokine interactions. Our results showed that CXCL12 binding is unusually slow and driven by the interplay between multiple binding epitopes. We also found that the amino terminus of the receptor played a key role in chemokine binding and activation by preventing chemokine dissociation. It was thought that chemokines initially bind receptors through interactions between the globular domain of the chemokine and the receptor amino terminus, which then guides the chemokine amino terminus into the transmembrane pocket of the receptor to initiate signaling. On the basis of our kinetic data, we propose an alternative mechanism in which the amino terminus of the chemokine initially forms interactions with the extracellular loops and transmembrane pocket of the receptor, which is followed by the receptor amino terminus wrapping around the core of the chemokine to prolong its residence time. These data provide insight into how ACKR3 competes and cooperates with canonical GPCRs in its function as a scavenger receptor.
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Schwartzkopff, Franziska, Frank Petersen, Tobias Alexander Grimm, and Ernst Brandt. "CXC chemokine ligand 4 (CXCL4) down-regulates CC chemokine receptor expression on human monocytes." Innate Immunity 18, no. 1 (November 18, 2010): 124–39. http://dx.doi.org/10.1177/1753425910388833.

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During acute inflammation, monocytes are essential in abolishing invading micro-organisms and encouraging wound healing. Recruitment by CC chemokines is an important step in targeting monocytes to the inflamed tissue. However, cell surface expression of the corresponding chemokine receptors is subject to regulation by various endogenous stimuli which so far have not been comprehensively identified. We report that the platelet-derived CXC chemokine ligand 4 (CXCL4), a known activator of human monocytes, induces down-regulation of CC chemokine receptors (CCR) 1, −2, and −5, resulting in drastic impairment of monocyte chemotactic migration towards cognate CC chemokine ligands (CCL) for these receptors. Interestingly, CXCL4-mediated down-regulation of CCR1, CCR2 and CCR5 was strongly dependent on the chemokine’s ability to stimulate autocrine/paracrine release of TNF-α. In turn, TNF-α induced the secretion CCL3 and CCL4, two chemokines selective for CCR1 and CCR5, while the secretion of CCR2-ligand CCL2 was TNF-α-independent. Culture supernatants of CXCL4-stimulated monocytes as well as chemokine-enriched preparations thereof reproduced CXCL4-induced CCR down-regulation. In conclusion, CXCL4 may act as a selective regulator of monocyte migration by stimulating the release of autocrine, receptor-desensitizing chemokine ligands. Our results stress a co-ordinating role for CXCL4 in the cross-talk between platelets and monocytes during early inflammation.
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Borroni, Elena M., Raffaella Bonecchi, and Annalisa M. VanHook. "Science Signaling Podcast: 30 April 2013." Science Signaling 6, no. 273 (April 30, 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 migration. Instead, signaling initiated by atypical chemokine receptors contributes to the immune response in other ways. The atypical chemokine receptor D6 is a scavenger that alters the chemokine gradient by binding to and degrading chemokines. Borroni and Bonecchi found that activation of a β-arrestin–dependent signaling pathway was necessary for D6 to act as a chemokine scavenger.
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Lim, Herman D., J. Robert Lane, Meritxell Canals, and Martin J. Stone. "Systematic Assessment of Chemokine Signaling at Chemokine Receptors CCR4, CCR7 and CCR10." International Journal of Molecular Sciences 22, no. 8 (April 19, 2021): 4232. http://dx.doi.org/10.3390/ijms22084232.

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Chemokines interact with chemokine receptors in a promiscuous network, such that each receptor can be activated by multiple chemokines. Moreover, different chemokines have been reported to preferentially activate different signalling pathways via the same receptor, a phenomenon known as biased agonism. The human CC chemokine receptors (CCRs) CCR4, CCR7 and CCR10 play important roles in T cell trafficking and have been reported to display biased agonism. To systematically characterize these effects, we analysed G protein- and β-arrestin-mediated signal transduction resulting from stimulation of these receptors by each of their cognate chemokine ligands within the same cellular background. Although the chemokines did not elicit ligand-biased agonism, the three receptors exhibited different arrays of signaling outcomes. Stimulation of CCR4 by either CC chemokine ligand 17 (CCL17) or CCL22 induced β-arrestin recruitment but not G protein-mediated signaling, suggesting that CCR4 has the potential to act as a scavenger receptor. At CCR7, both CCL19 and CCL21 stimulated G protein signaling and β-arrestin recruitment, with CCL19 consistently displaying higher potency. At CCR10, CCL27 and CCL28(4-108) stimulated both G protein signaling and β-arrestin recruitment, whereas CCL28(1-108) was inactive, suggesting that CCL28(4-108) is the biologically relevant form of this chemokine. These comparisons emphasize the intrinsic abilities of different receptors to couple with different downstream signaling pathways. Comparison of these results with previous studies indicates that differential agonism at these receptors may be highly dependent on the cellular context.
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Sanchez, Julie, J. Robert Lane, Meritxell Canals, and Martin J. Stone. "Influence of Chemokine N-Terminal Modification on Biased Agonism at the Chemokine Receptor CCR1." International Journal of Molecular Sciences 20, no. 10 (May 15, 2019): 2417. http://dx.doi.org/10.3390/ijms20102417.

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Leukocyte migration, a hallmark of the inflammatory response, is stimulated by the interactions between chemokines, which are expressed in injured or infected tissues, and chemokine receptors, which are G protein-coupled receptors (GPCRs) expressed in the leukocyte plasma membrane. One mechanism for the regulation of chemokine receptor signaling is biased agonism, the ability of different chemokine ligands to preferentially activate different intracellular signaling pathways via the same receptor. To identify features of chemokines that give rise to biased agonism, we studied the activation of the receptor CCR1 by the chemokines CCL7, CCL8, and CCL15(Δ26). We found that, compared to CCL15(Δ26), CCL7 and CCL8 exhibited biased agonism towards cAMP inhibition and away from β-Arrestin 2 recruitment. Moreover, N-terminal substitution of the CCL15(Δ26) N-terminus with that of CCL7 resulted in a chimera with similar biased agonism to CCL7. Similarly, N-terminal truncation of CCL15(Δ26) also resulted in signaling bias between cAMP inhibition and β-Arrestin 2 recruitment signals. These results show that the interactions of the chemokine N-terminal region with the receptor transmembrane region play a key role in selecting receptor conformations coupled to specific signaling pathways.
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Huang, Ziwei, Santosh Kumar, Won-Tak Choi, Navid Madani, Chang-Zhi Dong, Dongxiang Liu, Jun Wang, Jing An, and Joseph G. Sodroski. "A New Class of Chemokine Analogs as Useful Research Tools to Study Chemokine Receptor Function and Promising Therapeutic Agents." Blood 104, no. 11 (November 16, 2004): 3839. http://dx.doi.org/10.1182/blood.v104.11.3839.3839.

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Abstract Chemokine receptors play important roles in many physiological processes and are implicated in a wide range of human diseases including acute respiratory distress syndrome, allergic asthma, psoriasis, arthritis, multiple sclerosis, cancer, atherosclerosis and most notably AIDS. To enable the applications of chemokine ligands as probes of receptor biology and pharmacology, and inhibitors of diseases mediated by chemokine receptors, a major problem with the lack of receptor selectivity of these natural chemokines must be overcome. In this study, we have developed a chemical approach combining total protein synthesis and modular modifications to generate a new family of unnatural chemokines termed SMM-chemokines (which refer to synthetically and modularly modified chemokines) with designed receptor selectivity and affinity. A proof of the concept has been provided by applying this strategy to transform a very nonselective chemokine vMIP-II into new analogs with enhanced selectivity and potency for CXCR4 or CCR5, two principal coreceptors for HIV-1 entry. Such novel molecules have been shown subsequently to be valuable probes in gaining insights into receptor binding and signaling mechanisms, and as potent inhibitors to prevent HIV-1 entry and infection. These results strongly support the design concept of these SMM-chemokines and suggest that general applicability of this approach for studying and controlling other chemokine receptors and the diseases they mediate might be anticipated.
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BANAS, BERNHARD, BRUNO LUCKOW, MARCUS MÖLLER, CHRISTIANE KLIER, PETER J. NELSON, ERIK SCHADDE, MANFRED BRIGL, et al. "Chemokine and Chemokine Receptor Expression in a Novel Human Mesangial Cell Line." Journal of the American Society of Nephrology 10, no. 11 (November 1999): 2314–22. http://dx.doi.org/10.1681/asn.v10112314.

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Abstract. Chemokines are thought to play a pivotal role in mediating the selective migration of leukocytes into sites of tissue injury. The local production of chemokines by mesangial cells (MC) has been linked to inflammatory processes within the glomerulus. To study the chemokine biology of human MC, an immortalized human MC line was generated and then chemokine and chemokine receptor expression was examined in response to various proinflammatory stimuli. The results show that human MC have a specific and limited repertoire of chemokine expression. The stimulus-specific regulation of the chemokines monocyte chemoattractant protein-1 (MCP-1), regulated upon activation, normal T cell expressed and secreted (RANTES), interleukin-8 (IL-8), and IP-10 was demonstrated using RNase protection assays. Transcripts for the chemokines MIP-1α, MIP-1β, I-309, or lymphotactin could not be detected. The expression of CC chemokine receptors was investigated by reverse transcription-PCR and RNase protection assays. MC stimulated with interferon-γ (IFN-γ) expressed mRNA for the chemokine receptor CCR1. The expression could be further increased by activating the cells with a combination of tumor necrosis factor-α (TNF-α), IL-1β, and IFN-γ. Under these conditions, no mRNA for CCR2, CCR3, CCR4, CCR5, or CCR8 was detected. A comparison of the immortalized human mesangial cells with primary cells showed identical expression patterns of chemokine receptors. To demonstrate functional activity of chemokine receptors expressed by human MC, chemotaxis assays were performed. MC stimulated with a combination of TNF-α, IL-1β, and IFN-γ, but not unstimulated MC, migrated toward a RANTES gradient. Eotaxin did not enhance the migratory activity of human MC. In summary, a novel human mesangial cell line was established and the pattern of chemokine expression was examined. For the first time, the inducible expression of functionally active CCR1 by human MC was shown.
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Dissertations / Theses on the topic "Chemokine receptor"

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Wang, Jixin. "Bioinformatic analysis of chicken chemokines, chemokine receptors, and Toll-like receptor 21." Texas A&M University, 2006. http://hdl.handle.net/1969.1/4212.

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Chemokines triggered by Toll-like receptors (TLRs) are small chemoattractant proteins, which mainly regulate leukocyte trafficking in inflammatory reactions via interaction with G protein-coupled receptors. Forty-two chemokines and 19 cognate receptors have been found in the human genome. Prior to this study, only 11 chicken chemokines and 7 receptors had been reported. The objectives of this study were to identify systematically chicken chemokines and their cognate receptor genes in the chicken genome and to annotate these genes and ligand-receptor binding by a comparative genomics approach. Twenty-three chemokine and 14 chemokine receptor genes were identified in the chicken genome. The number of coding exons in these genes and the syntenies are highly conserved between human, mouse, and chicken although the amino acid sequence homologies are generally low between mammalian and chicken chemokines. Chicken genes were named with the systematic nomenclature used in humans and mice based on phylogeny, synteny, and sequence homology. The independent nomenclature of chicken chemokines and chemokine receptors suggests that the chicken may have ligand-receptor pairings similar to mammals. The TLR family represents evolutionarily conserved components of the patternrecognizing receptors (PRRs) of the innate immune system that recognize specific pathogen-associated molecular patterns (PAMPs) through their ectodomains (ECDs). TLR's ECDs contain 19 to 25 tandem copies of leucine-rich repeat (LRR) motifs. TLRs play important roles in the activation of pro-inflammatory cytokines, chemokines and modulation of antigen-specific adaptive immune responses. To date, nine TLRs have been reported in chicken, along with a non-functional TLR8. Two non-mammalian TLRs, TLR21 and TLR22, have been identified in pufferfish and zebrafish. The objectives of this study were to determine if there is the existence of chicken genes homologous to fish-specific TLRs, and if possible ligands of these receptors exist. After searching the chicken genome sequence and EST database, a novel chicken TLR homologous to fish TLR21 was identified. Phylogenetic analysis indicated that the identified chicken TLR is the orthologue of TLR21 in fish. Bioinformatic analysis of potential PAMP binding sites within LRR insertions showed that CpG DNA is the putative ligand of this receptor.
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Arnatt, Christopher Kent. "DEVELOPMENT OF ANTAGONISTS TARGETING CHEMOKINE RECEPTOR CCR5 AND THE CHEMOKINE RECEPTOR CCR5 – MU OPIOID RECEPTOR HETERODIMER." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/517.

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The chemokine receptor CCR5 (CCR5) plays an integral role within the inflammatory network of cells. Importantly, CCR5 is a mediator in several disease states and can be targeted using small molecule antagonists. Within this work, CCR5’s role in prostate cancer and HIV/AIDS has been exploited in order to develop potential therapeutics and probes. First, a series of novel compounds was designed by using pharmacophore-based drug design based upon known CCR5 antagonists and molecular modeling studies of the CCR5 receptor’s three-dimensional conformation. Once synthesized, these compounds were tested for their CCR5 antagonism and their anti-proliferative effects in several prostate cancer cell lines. The data from both the calcium mobilization studies and the anti-proliferation studies suggests that the compounds synthesized have activity as CCR5 antagonists and as anti-proliferative agents in certain prostate cancer cell lines. In addition, a bivalent ligand containing both a mu opioid receptor (MOR) and a CCR5 antagonist pharmacophore was designed and synthesized in order to study the pharmacological profile of the putative CCR5-MOR heterodimer and its relation with NeuroAIDS. The structural-activity relationship between the bivalent ligand and the heterodimer was studied with radio-ligand binding assays, functional assays, HIV-1 fusion assays, cell fusion assays, and in silico molecular dynamics. The subsequent bivalent ligand was proven to be a potent inhibitor in both an artificial cell fusion assay mimicking HIV invasion and a native HIV-1 invasion assay using live virus. In all, two novel sets of compounds were synthesized that targeted either CCR5 or the CCR5-MOR heterodimer. For the CCR5 antagonists, as leads for prostate cancer therapeutics, further work needs to be done to ascertain and develop their structure-activity-relationship. This library of novel compounds was shown as promising leads as CCR5 and anti-prostate cancer agents. The bivalent ligand targeting the CCR5-MOR heterodimer proved to be a potent and tissue-specific inhibitor for neuroAIDS where the known treatment, maraviroc, is less efficacious and fails to inhibit virus entry in the presence of morphine. Both projects illustrate the roles that CCR5 plays in these two unique diseases.
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Davis, Christopher Nathan. "Mammalian and viral chemokines provide insight into the mechanism of chemokine receptor activation." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006481.

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Kiss, Debra Lois. "Regulation of the Chemokine Receptors CXCR4, CXCR7 , and the Androgen Receptor in Prostate Cancer." Thesis, Griffith University, 2013. http://hdl.handle.net/10072/367690.

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The chemokine receptor CXCR4 contributes to tumour cell migration and invasion during the progression of prostate cancer. In particular, this pathway is central to the metastasis of prostate cancer to the bone marrow. Limited therapeutic options exist for prostate cancer patients who have progressed to advanced metastatic disease, and pharmacological interference of the chemokine network may serve to control tumour cell dissemination and the establishment of metastasis. A more detailed knowledge of the mechanisms regulating chemokine receptors is required, in order to further characterise and explore the capacity and effectiveness of targeting these pathways for therapeutic intervention in prostate cancer. Here, the regulation of CXCR4 protein expression and function was investigated in relation to androgens and the extracellular matrix. Accumulating evidence of CXCR4 regulation by androgens and the androgen receptor have indicated that androgens not only promote the growth and development of prostate cancer, but may actively contribute to the metastatic progression of prostate through modulation of the chemokine network. In the current study, the endogenous protein expression and functionality of the androgen receptor were firstly characterised in the androgen-insensitive prostate cancer cell lines DU145 and PC3, using the androgen-sensitive LNCaP cells as a basis for comparison. Investigations were performed using two-dimensional culture in conjunction with the more physiologically relevant three-dimensional in vitro culture model.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Eskitis Institute for Cell and Molecular Therapies
Science, Environment, Engineering and Technology
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Khan, Abid. "CXCR4 chemokine receptor antagonists : new metallodrugs." Thesis, University of Hull, 2009. http://hydra.hull.ac.uk/resources/hull:10418.

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Chemokine receptors are a target of growing interest for new therapeutic drugs, as their role in multiple disease states has been demonstrated. The CXCR4/ CXCL12 pairing has been implicated in HIV and cancer, as well as chronic inflammatory diseases, including asthma and rheumatoid arthritis. HIV uses CXCR4 or CCR5 receptors in the key binding step of the infection process, leading to the idea that drugs could be developed to block this interaction. Cancer metastasis has also been linked to cellular communication via the chemokine pathways and hence, receptor antagonists could potentially inhibit this important pathway of disease progression. Small synthetic CXCR4 antagonists exist including AMD3100 (Mozobil®/Plerixafor), which has been identified as a potent CXCR4 antagonist exhibiting anti-HIV, anti-inflammatory and anti-tumour activity. Configurationally restricted analogues of AMD3100 complexed to metal ions have improved binding characteristics compared to AMD3100 and its metal complexes. Herein we report the binding of a new class of cyclen, cyclam and tris-cyclam based complexes in vitro. Compounds competed effectively in anti-CXCR4 competition assays with the tricyclam linear complex displaying improved binding characteristics. The difference in activity of the compounds is discussed in relation to the different possible binding interactions that are occurring. Furthermore, a monocyclam derivative conjugated to biotin competed effectively in competition with a CXCR4 mAb, however could not directly be detected via a fluorescent conjugated streptavidin molecule. Our most potent compound to date, copper(II) cross-bridged bicyclam was found to have a significant higher relative residence time in CXCR4 compared to AMD3100 and copper(II) AMD3100 in vitro. Moreover, copper(II) cross-bridged bicyclam was able to totally block CXCL12 induced and partially block serum induced, invasion of CXCR4 positive cancer cells with a higher potency than AMD3100 and copper(II) AMD3100. This shows the potential of using such a drug in the clinic. Using CXCR4 mutants, it has been shown that CXCR4 defective degradation and recycling increases invasion in breast cancer cells. Moreover the development of a multicellular tumour spheroid (MTS) is reported that could be used as a preclinical model in the evaluation of the anti-cancer activity of CXCR4 antagonists.
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Wavre, Silene Tuija. "Endocytic regulation of chemokine receptor expression." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1446114/.

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The activity of stimulated cell surface signalling receptors is frequently regulated by endocytosis, which provides a mechanism to internalise and either degrade or reprogram the protein. Clathrin-mediated endocytosis (CME) is one of the principal mechanisms responsible for these events. Although clathrin and many of its associated proteins are relatively well characterised, many aspects of how CME operates are yet to be established. In particular, the early steps of internalisation, the formation of clathrin-coated pits (CCPs) and the mechanism by which receptors are recruited into CCPs remain controversial. This thesis investigates the early events of CME occurring at the plasma membrane using as a model various cell lines expressing CC Chemokine receptor 5 (CCR5), a G-protein coupled receptor (GPCR). Upon agonist binding, CCR5 undergoes rapid phosphorylation by a GPCR kinase (GRK) and protein kinase C (PKC) on four C-terminal serines, p-arrestin is subsequently recruited to the receptor, abrogates CCR5 interaction with the G- protein and links the receptor to the endocytic machinery by binding to AP-2 and clathrin. Using confocal immunofluorescence microscopy and electron microscopy, I show that, on agonist binding, CCR5 relocates in the plasma membrane and clusters into flat clathrin lattices. CCPs were observed to invaginate at the edge of these lattices and proteins from the endocytic machinery were identified by immunolabelling within these domains. As C-terminal serine phosphorylation has been found to be important for efficient agonist-induced internalisation of CCR5, the requirement for specific serines for plasma membrane relocation, association with clathrin lattices and endocytosis were analysed. A mutant lacking all serines failed to be recruited into flat clathrin lattices. Further analysis showed that specific GRK phosphorylation of CCR5 was sufficient for this recruitment, suggesting a distinct role for different kinases in receptor desensitisation and internalisation. This study brings new insights into the mechanism of recruitment of activated GPCRs into CCPs and reveals the importance of flat clathrin lattices in the formation of endocytic clathrin-coated vesicles and CME. Part of the results presented in this thesis have been published (Signoret et al., 2005) (see appendix).
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Fouillet, Antoine. "Cytokines regulation of chemokine and chemokine receptor in relation to multiple sclerosis." Thesis, Sheffield Hallam University, 2008. http://shura.shu.ac.uk/19675/.

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Expression of chemokines CXCL10 and CCL2 is elevated within inflammatory lesions in the central nervous system (CNS) of multiple sclerosis (MS) patients, particularly in astrocytes. These chemokines play a critical role in the recruitment of inflammatory cells into the CNS during inflammation. However, the cerebrospinal fluid of MS patients also shows high levels of CXCL10 at the time of relapse but by contrast CCL2 is decreased. In the present study, the mechanisms controlling the synthesis and release of these two chemokines in MS were assessed in vitro using primary human brain astrocytes isolated from MS and non-MS individuals. Pro-inflammatory cytokines (interleukin-1beta , tumour necrosis factor and interferon-gamma) increased the expression of both CCL2 and CXCL10 by astrocytes at the mRNA and protein level, as determined by real time PCR and enzyme linked immunosorbent assays (ELISA), respectively. CCL2 binding to astrocytes was then determined to evaluate any autocrine action on astrocytes in a single astrocyte preparation. CCL2 bound constitutively and following cytokine treatment. CCL2-binding was not the result of the interaction with its receptor since astrocytes did not express CCR2 on this astrocyte culture. CCR2-independent binding of CCL2 was confirmed by the absence of intracellular signalling, evidenced by the lack of calcium influx as well as of Erk and Akt phosphorylation, in CCL2-treated astrocytes. Even though astrocytes expressed CXCR3, similar negative results on calcium influx and downstream signalling pathways were observed for CXCL10. D6 chemokine decoy receptor expression was then assessed in vitro and in situ to further investigate the mechanism(s) of chemokine binding to astrocytes. Cultured astrocytes constitutively expressed the D6 decoy receptor at the mRNA and protein level, but levels were unchanged following cytokine treatment. D6 was expressed in situ in MS normal appearing white matter and in control brain tissue, at both the mRNA and protein level. D6 expression was detected on neurons and microglia but not astrocytes using imunohistochemical methods. Incubation of frozen brain sections with biotinylated CCL2 resulted in partial co-localisation with D6 staining. Altogether, these results suggest a role for astrocytes in regulating inflammation through synthesis and secretion of CCL2 and CXCL10. Subsequently, CCL2 binding to astrocytes, either by binding to D6 decoy receptor or by alternative mechanisms, may establish a chemokine gradient in the CNS, and direct the migration of leukocytes.
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Eltayeb, Sana. "Chemokine receptor expression and function in experimental autoimmune neuroimflammation /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-197-5/.

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Duchesnes, Cecile Emmanuelle. "Molecular characterisation of the chemokine receptor CCR3." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407171.

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Martinelli, Roberta. "Molecular characterisation of the chemokine receptor CCR2." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398841.

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Books on the topic "Chemokine receptor"

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Meucci, Olimpia. Chemokine receptors and neuroAIDS: Beyond co-receptor function and links to other neuropathologies. New York: Springer, 2010.

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Masters, Jennefer. Myxoma virus induced activation of CC-chemokine receptor 5 (CCR5). Ottawa: National Library of Canada, 2000.

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1956-, Moser Bernhard, Letts Gordon L, and Neote Kuldeep, eds. Chemokine biology: Basic research and clinical application. Basel: Birkhäuser, 2005.

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Richard, Horuk, ed. Chemokine receptors. San Diego: Academic Press, 1997.

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I, Proudfoot Amanda E., Wells Timothy N. C, and Power Christine, eds. Chemokine protocols. Totowa, N.J: Humana Press, 2000.

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Harrison, Jeffrey K., and Nicholas W. Lukacs, eds. The Chemokine Receptors. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-020-1.

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K, Harrison Jeffrey, and Lukacs Nicholas W, eds. The chemokine receptors. Totowa, N.J: Humana, 2007.

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Ubogu, Eroboghene E., and Astrid E. Cardona. Chemokines: Methods and protocols. New York: Humana Press, 2013.

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Caroline, Hébert, ed. Chemokines in disease: Biology and clinical research. Totowa, N.J: Humana Press, 1999.

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1950-, O'Brien Thomas, ed. Chemokine receptors and AIDS. New York: Marcel Dekker, 2002.

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Book chapters on the topic "Chemokine receptor"

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Islam, Sabina A., Benjamin D. Medoff, and Andrew D. Luster. "Chemokine and Chemokine Receptor Analysis." In Manual of Molecular and Clinical Laboratory Immunology, 343–56. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555818722.ch37.

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Horuk, Richard. "Chemokine Receptor CCR1." In Encyclopedia of Signaling Molecules, 1065–74. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_406.

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Blay, Jonathan. "Chemokine Receptor CXCR4." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1067-3.

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Horuk, Richard. "Chemokine Receptor CCR1." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_406-1.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Chemokine Receptor CCR1." In Encyclopedia of Signaling Molecules, 386–95. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_406.

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Blay, Jonathan. "Chemokine Receptor CXCR4." In Encyclopedia of Cancer, 932–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_1067.

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Baird, Anne-Marie, Kenneth J. O’Byrne, and Steven G. Gray. "Epigenetic Regulation of Chemokine/Chemokine Receptor Expression." In Methods in Molecular Biology, 185–201. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_12.

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Garin, Alexandre, Zoë Johnson, Aurelie Hermant, Fanny Beltran, Yann Ratinaud, Alexandra Michel, Sonja Krohn, et al. "Chemokine Receptor Antagonist Development." In Methods in Molecular Biology, 67–92. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_6.

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Richmond, Ann, Guo Huang Fan, Punita Dhawan, and Jinming Yang. "How Do Chemokine/Chemokine Receptor Activations Affect Tumorigenesis?" In Novartis Foundation Symposia, 74–91. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470856734.ch6.

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Newcomb, Elizabeth W., and David Zagzag. "HIF-1 Regulation of Chemokine Receptor Expression." In Chemokine Receptors in Cancer, 47–61. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-267-4_3.

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Conference papers on the topic "Chemokine receptor"

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"Impact of Heparan Sulphate Binding Domain of Chemokine CCL21 to Migration of Breast Cancer Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0132.

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Lymph node metastasis constitutes a key event in breast cancer progression. Chemokines are small proteins, which can promote metastatic spread by inducing cancer cell migration and invasion. Chemokine function is dependant upon their binding to both cell surface heparan sulphate (HS) molecules and to their specific receptor. Our group has demonstrated a significant increase in chemokine receptor CCR7 expression in cancerous breast epithelia compared to healthy controls. This study is designed to test the hypothesis that a non-HS binding forms of chemokine CCL21 can disrupt the normal response to CCL21, therefore reducing the metastasis of CCR7-expressing cancer cells. Truncated CCL21 chemokine (Δ98- 134 c-terminal basic extension), was synthesised to investigate a possible linkage between chemokine binding capacity and cell activation. Wild type (WT) and mutant-CCL21 were tested for their ability to stimulate a dose-dependent increase in intracellular-free calcium in peripheral blood mononuclear cell (PBMC) and breast cancer epithelial cells MDA-MB-231. Mutant-CCL21 at concentrations 5 and 10nM showed potential to mobilise Ca2+ at levels similar to that produced by WT-CCl21. A series of experiments was performed to determine how deletion of the HS-binding site altered the ability of CCL21 to stimulate chemotaxis within a concentration gradient generated by free solute diffusion. PBMC stimulated to migrate by wild-type CCL21 was not significantly different from that stimulated by mutant (P> 0.05). Similar results were observed in assays using MDA-MB-231 cells. A further series of experiments was performed to compare the potential of WT and mutant-CCL21 to stimulate the migration of cells across endothelium. In contrast to results for trans-filter migration, it was found that the non HSbinding mutant stimulated no increased in transendothelial cell migration above the background at each of the tested concentrations, 10, 30 and 50 nM respectively (P>0.05). However, WT-CCL21 stimulated significant increased PBMC migration at each of the tested concentration (all P <0.001). Furthermore, the effect of heparin on chemotactic properties of WT and mutant- CCL21 was examined. Interestingly, heparin (250 µg/ml) completely inhibit the chemotaxis mediated by WT-CCL21 (5nM) (P < 0.001), whereas it did not inhibit the chemotaxis at concentrations 100, 250 & 500 µg/ml in response to mutant CCL21 (5nM) (P > 0.05). Similar assay will be performed using MDA-MB-231 cells. Work is ongoing to characterise the biophysical properties of mutant-CCL21 and determine its potential role for a therapeutic blockade of the migration of breast cancer cells in-vivo. Our primarily data showed that mutant CCL21 in xenograft brain tumor models showed substantial inhibition of tumour growth. Our results indicate that truncated CCL21 chemokine might be a potential preventive biofactor for human breast cancer metastasis by targeting chemokine receptor genes.
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Yu, Yingyan, Eva Brudy, Rabea Imker, Cornelia Dalibor, Oliver Eickelberg, and Susanne Krauss-Etschmann. "Upregulation Of Pulmonary Chemokine Receptor 2 (CCR2) Positive T Cells And Their Chemokine Receptors Profile In Bleomycin-Induced Lung Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5397.

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Chen, Huanhuan, Serena Tucci, Zeynep Gümüs, Xiling Shen, and Steven M. Lipkin. "Abstract 5207: The chemokine 25 and chemokine receptor 9 axis suppresses colon cancer invasion and metastasis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5207.

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Weiß, T., and A. Beck-Sickinger. "Etablierung eines Assays-Systems für den chemokine-like receptor (CMKLR1)." In Abstracts des Adipositas-Kongresses 2020 zur 36. Jahrestagung der Deutschen Adipositas Gesellschaft e.V. (DAG). © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1714477.

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Halfhide, CP, S. Brearey, PS McNamara, JA Hunt, D. Howarth, J. Cummerson, RL Smyth, and BF Flanagan. "Chemokine Receptor Expression in Human Respiratory Syncytial Virus (RSV) Bronchiolitis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5989.

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Kidd, LaCreis R., Sydney C. Beache, Jie Zheng, Guy Brock, James W. Lillard, James Rudd, and Kevin S. Kimbro. "Abstract 2780: Chemokine and chemokine receptor genetic variants as predictors of aggressive prostate cancer among European-American men." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2780.

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Wei, Xiao-Lan, Jing Zhang, and Zhi-Hong Mo. "Regulation of chemokine receptor CXCR4 in HepG2 cell adhesion sensing by QCM." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6029075.

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Davies, Ceri, Jo Ann Rhodes, Peter Barnes, and Louise Donnelly. "Elevated CCL2 responses in COPD and attenuation by selective chemokine receptor antagonists." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3900.

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Bonelli, M., A. Puchner, L. Goeschl, S. Hayer, B. Niederreiter, JS Smolen, C. Scheinecker, and S. Blueml. "FRI0064 Chemokine receptor 6 modulates arthritis in a t cell dependent manner." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5107.

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Singh, Rajesh, Pranav Gupta, William E. Grizzle, James W. Lillard, and Shailesh Singh. "Abstract 5121: Differential expression of CC chemokine receptor-9 in prostate cancer." 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.am2013-5121.

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Reports on the topic "Chemokine receptor"

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Reshef, Ran. Chemokine Receptor Signatures in Allogeneic Stem Cell Transplantation. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada610688.

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Reshef, Ran. Chemokine Receptor Signatures in Allogeneic Stem Cell Transplantation. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada620593.

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McCarthy, James B. Chemokine Receptors and Integrin Function in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada412790.

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McCarthy, James B. Chemokine Receptors and Integrin Function in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2000. http://dx.doi.org/10.21236/ada391087.

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Blondelle, Sylvie E. Development of Peptide Antagonists of Chemokine Receptors Involved in Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada432047.

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Blondelle, Sylvie E. Development of Peptide Antagonists of Chemokine Receptors Involved in Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada434632.

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