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趋化因子受体 ACKR3/CXCR7 在以病毒相关癌症为重点的癌症中对 CXCL12 介导的作用的相关性。

The relevance of the chemokine receptor ACKR3/CXCR7 on CXCL12-mediated effects in cancers with a focus on virus-related cancers.

机构信息

Univ. Paris-Sud, Laboratoire "Cytokines, Chemokines and Immunopathology", UMR_S996, 32, rue des Carnets, Clamart F-92140, France; INSERM, Univ. Paris-Sud, Laboratory of Excellence in Research on Medication and Innovative Therapeutics (LERMIT), Clamart F-92140, France.

Univ. Paris-Sud, Laboratoire "Cytokines, Chemokines and Immunopathology", UMR_S996, 32, rue des Carnets, Clamart F-92140, France; INSERM, Univ. Paris-Sud, Laboratory of Excellence in Research on Medication and Innovative Therapeutics (LERMIT), Clamart F-92140, France.

出版信息

Cytokine Growth Factor Rev. 2014 Jun;25(3):307-16. doi: 10.1016/j.cytogfr.2014.04.006. Epub 2014 May 9.

DOI:10.1016/j.cytogfr.2014.04.006
PMID:24853339
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.

摘要

最近的研究强调了理解 CXCL12 介导的癌症作用的分子决定因素的重要性。以前曾认为 CXCL12 仅与 CXCR4 相互作用,但其也与高亲和力结合 CXCR7(最近更名为 ACKR3),后者属于一种非典型趋化因子受体家族,其成员不能激活 Gαi 蛋白,但与β-arrestin 相互作用。除了控制 CXCL12 生物利用度的能力外,ACKR3 还可以增强或抑制 CXCR4 介导的信号转导和活性。鉴于最近的发现,我们研究了 ACKR3 在癌症中的作用,包括一组与病毒相关的癌症。

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