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Chemo kine receptors

Daelemans, D., Schols, D., Witvrouw, M., Rannecouque, C., Hatse, S., Door-EN, S.V., Hamy, F., Klimkait, X, Clercq, E.D., and Vandamme, A.-M. A second target for the peptoid Xat/transactivation response element inhibitor CGP64222 Inhibition of human immunodeficiency virus replication by blocking CXC-chemo-kine receptor 4-mediated virus entry. [Pg.29]

The literature on chemokines in transplantation has been extensively reviewed in recent years (7-9). In this chapter, we focus on a limited number of chemo-kine receptors where evidence for a functional role has been verified. From the plethora of chemokine receptors, this has been demonstrated for CXCR1/2 in reperfusion injury and for CCR1, CCR5, and CXCR3 during acute and chronic allograft rejection. [Pg.140]

Haringman JJ, Smeets TJ, Reinders-Blankert P, Tak PP. Chemokine and chemo-kine receptor expression in paired peripheral blood mononuclear cells and synovial tissue of patients with rheumatoid arthritis, osteoarthritis, and reactive arthritis. Ann Rheum Dis 2006 65(3) 294-300. [Pg.186]

Wang JM, Oppenheim JJ. Interference with the signaling capacity of CC chemo-kine receptor 5 can compromise its role as an HIV-1 entry coreceptor in primary T lymphocytes. J Exp Med 1999 190(5) 591-595. [Pg.288]

Ai, L. S., and Liao, F. (2002). Mutating the four extracellular cysteines in the chemo-kine receptor CCR6 reveals their differing roles in receptor trafficking, ligand binding, and signaling. Biochem. 41, 8332-8341. [Pg.432]

Murphy, P. M. (2002). International Union of Pharmacology. XXX. Update on chemo-kine receptor nomenclature. Pharmacol. Rev. 54, 227-229. [Pg.440]

L., Gerard, N. P., Wyatt, R., Choe, H., Parolin, G., Ruffing, N., Borsetti, A., Cardoso, A. A., Desjardin, E., Newman, W., Gerard, C., and Sodroski, J. (1996a). GDI-induced interaction of primary HIV-1 gpl20 glycoproteins vdth the chemo-kine receptor CCR-5. Nature 384, 179-183. [Pg.444]

Car der L, Har tley O, Dubois-Dauplrhr M, Kr ause KH (2005) Chemo-kine receptors m die central nerwous system Role in brain uiflam-madon and neurodegeneradve diseases. Brain Reseai ch Reviews 48 16-42. [Pg.491]

Cartier L, Hartley O, Dubois-Dauphin M, Krause KH (2005) Chemo-kine receptors in the central nervous system Role in brain inflammation and neurodegenerative diseases. Brain Research Reviews 48 16-12. [Pg.491]

Angiotensin-converting enzyme inhibition down-regulates the pro-atherogenic chemo-kine receptor 9 (CCR9)-chemokine ligand 25 (CCL25) axis. J Biol Chem 285 23496-23505... [Pg.298]

Banas B et al (1999) Chemokine and chemo-kine receptor expression in a novel human mesangial cell line. J Am Soc Nephrol 10(11) 2314-2322... [Pg.101]

CCR3 Receptor Structure. Chimera studies of CCR3 and CCRl receptors show that the N-terminal segments of CCR3 appear to be important for eotaxin binding (77). However, eotaxin remained an effective agonist at this chimeric receptor in either calcium flux or chemotaxis assays. These data are consistent with a multisite model for chemokine-chemo-kine receptor interaction. [Pg.149]

Nelson PJ, Krensky AM. Chemokines, chemo-kine receptors, and allograft rejection. Immunity 2001 14 377-386. [Pg.380]

Yoganathan K, Rossant C, Glover R P, et al. (2004). Inhibition of the hnman chemo-kine receptor CCR5 by variecolin and variecolol and isolation of fonr new variecolin analogues, emericolins A-D, from Emericella aurantiobrunnea. J. Nat. Prod. 67 1681-1684. [Pg.567]

Loetscher M, Loetscher P, Brass N, Meese E, Moser B. Lymphocyte-specific chemo-kine receptor CXCR3 regulation, chemokine binding and gene localization. Eur J Immunol 1998 28 3696-3705. [Pg.110]

Lane BR, Markovitz DM, Woodford NL, Rochford R, Strieter RM, Coffey MJ. TNF-alpha Inhibits HIV-1 replication in peripheral blood monocytes and alveolar macrophages by inducing the production of RANTES and decreasing C-C chemo-kine receptor 5 (CCR5) expression. J Immunol 1999 163 3653-3661. [Pg.188]

Gao JL, Wynn TA, Chang Y, et al. Impaired host defense, hematopoiesis, granulomatous inflammation and type 1-type 2 cytokine balance in mice lacking CC chemo-kine receptor 1. J Exp Med 1997 185 1959-1968. [Pg.258]

Recent literature supports that inflammatory cells can be activated by oxidative stress, thereby causes the chronic infections and associated inflammation may be further enhanced that leads to the process of cancer formation [46,47]. Inflammatory cytokines such as tumor necrosis factor (TNF), interleukin-1 (lL-1), lL-6, and chemokines such as lL-8, CXC, and chemo-kine receptor 4 (CXCR4) are the important products produced by inflammatory cells [29]. [Pg.123]

The assay is conveniently performed in TransweU insets (pore size 8 [im) on which endothelial cells or cells of interest expressing scavenging chemo-kine receptors are grown to confluence. To start the experiment, the culture... [Pg.92]

Cheshire D, Kindon N, Stocks M (2004) Sulphonamide compounds that modulate chemo-kine receptor activity (CCR4). PCT Int Pat WO 2004108690... [Pg.552]


See other pages where Chemo kine receptors is mentioned: [Pg.285]    [Pg.301]    [Pg.3112]    [Pg.132]    [Pg.21]    [Pg.172]    [Pg.95]    [Pg.53]    [Pg.7]    [Pg.85]    [Pg.92]    [Pg.335]    [Pg.424]    [Pg.435]    [Pg.643]    [Pg.293]    [Pg.86]   


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