Induction of cellular migration is the primary effect of chemokine receptor activation. However, several chemokine receptor-like proteins bind chemokines without subsequent induction of intracellular signalling and chemotaxis. It has been suggested that they act as chemokine scavengers, which may control local chemokine levels and contribute to the function of chemokines during inflammation. This has been verified for the chemokine-like receptor proteins D6 and DARC as well as CCX-CKR. Here, we provide evidence for an additional biological function of human (h)CCX-CKR.
Inhibition of CXCR3-mediated chemotaxis by the human chemokine receptor-like protein CCX-CKR / Vinet, Jonathan; van Zwam, M; Dijkstra, I. M; Brouwer, N; van Weering, H. R. J; Watts, A; Meijer, M; Fokkens, M. R; Kannan, V; Verzijl, D; Vischer, H. F; Smit, M. J; Leurs, R; Biber, K; Boddeke, H. W. G. M.. - In: BRITISH JOURNAL OF PHARMACOLOGY. - ISSN 0007-1188. - 168:6(2013), pp. 1375-1387. [10.1111/bph.12042]
Inhibition of CXCR3-mediated chemotaxis by the human chemokine receptor-like protein CCX-CKR
VINET, JONATHAN;
2013
Abstract
Induction of cellular migration is the primary effect of chemokine receptor activation. However, several chemokine receptor-like proteins bind chemokines without subsequent induction of intracellular signalling and chemotaxis. It has been suggested that they act as chemokine scavengers, which may control local chemokine levels and contribute to the function of chemokines during inflammation. This has been verified for the chemokine-like receptor proteins D6 and DARC as well as CCX-CKR. Here, we provide evidence for an additional biological function of human (h)CCX-CKR.
| File | Dimensione | Formato | |
|---|---|---|---|
|
Vinet et al 2012b.pdf
Accesso riservato
Tipologia:
VOR - Versione pubblicata dall'editore
Dimensione
1.99 MB
Formato
Adobe PDF
|
1.99 MB | Adobe PDF | Visualizza/Apri Richiedi una copia |
Pubblicazioni consigliate
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris
