Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2170466 | Cytokine & Growth Factor Reviews | 2014 | 10 Pages |
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.
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Authors
Christelle Freitas, Aude Desnoyer, Floriane Meuris, Françoise Bachelerie, Karl Balabanian, Véronique Machelon,