| Literature DB >> 24853339 |
Christelle Freitas1, Aude Desnoyer1, Floriane Meuris1, Françoise Bachelerie1, Karl Balabanian2, Véronique Machelon3.
Abstract
Recent studies have highlighted the importance of understanding the molecular determinants of CXCL12-mediated effects in cancers. Once previously thought to interact exclusively with CXCR4, CXCL12 also binds with high affinity to CXCR7 (recently renamed ACKR3), which belongs to an atypical chemokine receptor family whose members fail to activate Gαi proteins but interact with β-arrestins. In addition to its capacity to control CXCL12 bioavailability, ACKR3 can either enhance or dampen CXCR4-mediated signaling and activity. In light of the most recent findings, we have examined the role of ACKR3 in cancer, including a subset of virus-related cancers.Entities:
Keywords: ACKR3/CXCR7; CXCL12/SDF-1; CXCR4; Cancer; Virus
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Year: 2014 PMID： 24853339 DOI： 10.1016/j.cytogfr.2014.04.006
Source DB: PubMed Journal: Cytokine Growth Factor Rev ISSN： 1359-6101 Impact factor: 7.638