Atypical chemokine receptors: from silence to sound
Atypical chemokine receptors: from silence to sound
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DOI：
10.1042/bst20120246
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发表时间：
2013-02-01
影响因子：
3.9
通讯作者：
Borroni, Elena M.
中科院分区：
文献类型：
--
作者：
Cancellieri, Cinzia;Vacchini, Alessandro;Borroni, Elena M.
ACR（非典型趋化因子受体）最初被称为“沉默”受体的基础上，缺乏信号和功能活动，通常观察到与传统的趋化因子受体。虽然ACR不直接诱导细胞迁移，但它们通过降解、胞吞转运或其同源配体的局部浓缩在组织中形成趋化因子梯度来间接控制白细胞募集。最近的证据还表明，这些生物活性是由G蛋白独立的，β-arrestin依赖的信号传导事件支持的。在本文章中，我们回顾了目前的知识结构和信号特性的ACR，改变了我们的看法，这整个类受体从沉默的内源性β-arrestin偏信号受体。
ACRs (atypical chemokine receptors) were initially referred to as 'silent' receptors on the basis of a lack of signalling and functional activities that are typically observed with conventional chemokine receptors. Although ACRs do not directly induce cell migration, they indirectly control leucocyte recruitment by shaping chemokine gradients in tissues through degradation, transcytosis or local concentration of their cognate ligands. Recent evidence also suggests that these biological activities are supported by G-protein-independent, beta-arrestin-dependent signalling events. In the present article, we review current knowledge on structural and signalling properties of ACRs that are changing our view on this entire class of receptors from silent to endogenous beta-arrestin-biased signalling receptors.