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The mechanisms regulating the subcellular localization of AID

机译：调节AID亚细胞定位的机制

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Activation induced deaminase (AID) is a unique enzyme that directly introduces mutations in the immunoglobulin genes to generate antibody diversity during the humoral immune response. Since this mutator enzyme poses a measurable risk of off-target mutation, which can be deleterious or transforming for a cell, several regulatory mechanisms exist to control its activity. At least three of these mechanisms affect AID subcellular localization. It was recently found that AID is actively imported into the nucleus, most likely through importin-α/β recognizing a structural nuclear localization signal. However, AID is largely excluded from the nucleus in steady state thanks to two mechanisms. In addition to nuclear export through the exportin CRM1, a mechanism retaining AID in the cytoplasm exists. Cytoplasmic retention hinders the passive diffusion of AID into the nucleus playing an important role in the nuclear exclusion of AID. Subcellular localization of AID also determines its stability. The regulation of the nuclear fraction of AID by these many mechanisms has functional implications for antibody diversification.
机译：激活诱导的脱氨酶（AID）是一种独特的酶，可直接在免疫球蛋白基因中引入突变，从而在体液免疫应答过程中产生抗体多样性。由于这种突变酶带来了可测量的脱靶突变风险，这种脱靶突变可能对细胞有害或转化，因此存在几种调节机制来控制其活性。这些机制中的至少三种会影响AID亚细胞定位。最近发现，AID很可能通过识别结构核定位信号的importin-α/β主动地导入细胞核。但是，由于两种机制，AID在稳定状态下基本上被排除在原子核之外。除了通过exportin CRM1进行核输出外，还存在在细胞质中保留AID的机制。细胞质保留阻止了AID被动扩散到细胞核中，在AID的核排斥中起着重要作用。 AID的亚细胞定位也决定了其稳定性。通过这些许多机制对AID的核部分进行调节对抗体多样化具有功能上的意义。

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