Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.
Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.
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B细胞中的突变，Kataegis和易位：了解有助于混杂活性。
DOI：
10.1038/nri.2016.2
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发表时间：
2016-03
期刊：
影响因子：
--
通讯作者：
Di Noia JM
中科院分区：
文献类型：
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作者：
Casellas R;Basu U;Yewdell WT;Chaudhuri J;Robbiani DF;Di Noia JM
当B细胞参与免疫应答时，它们会表达激活诱导的胞苷脱氨酶（AID）来启动免疫球蛋白基因的超突变和重组，这对于有效识别和清除病原体是至关重要的过程。然而，必须在B细胞中对AID进行严格控制，以尽量减少脱靶突变，因为脱靶突变可导致染色体易位以及B细胞恶性肿瘤（如淋巴瘤）的发生。最近的基因组学和生物化学分析已经开始解开AID介导的脱氨作用如何靶向免疫球蛋白基因之外的关键问题。在此，我们讨论作为AID杂乱活性关键驱动因素而出现的转录和拓扑特征。
As B cells engage in the immune response they express the deaminase AID to initiate the hypermutation and recombination of immunoglobulin genes, which are crucial processes for the efficient recognition and disposal of pathogens, However, AID must be tightly controlled in B cells to minimize off-targeting mutations, which can drive chromosomal translocations and the development of B cell malignancies, such as lymphomas. Recent genomic and biochemical analyses have begun to unravel the crucial question of how AID-mediated deamination is targeted outside immunoglobulin genes. Here, we discuss the transcriptional and topological features that are emerging as key drivers of AID promiscuous activity.