RNA rewriting, recoding, and rewiring in human disease.
RNA rewriting, recoding, and rewiring in human disease.
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DOI：
10.1016/j.molmed.2015.07.001
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发表时间：
2015-09
影响因子：
13.6
通讯作者：
M. Zipeto;Qingfei Jiang;E. Melese;C. Jamieson
中科院分区：
文献类型：
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作者：
M. Zipeto;Qingfei Jiang;E. Melese;C. Jamieson
ADAR(作用于RNA的腺苷脱氨酶)编辑酶催化腺苷脱氨为肌苷(A-to-I)，这是一种转录后修饰，改变了编码和非编码RNA的稳定性和功能。ADAR编辑酶，如ADAR1，最近已被证明在正常干细胞维持中发挥关键作用。虽然ADAR突变与遗传性自身免疫性疾病(如艾卡迪-古蒂埃综合征)有关，但ADAR拷贝数改变和编辑酶激活与一系列恶性肿瘤的进展有关。在这篇综述中，我们讨论了将异常的A-to-I编辑与癌症和其他退行性疾病联系起来的证据，以及可能被新的治疗策略作为靶点的机制。
ADAR (adenosine deAminase acting on RNA) editases catalyze the deamination of adenosine to inosine (A-to-I), a post-transcriptional modification that alters coding and non-coding RNA stability and function. ADAR editases such as ADAR1 have recently been shown to play a key role in normal stem cell maintenance. While ADAR mutations are associated with hereditary autoimmune diseases such as Aicardi–Goutières syndrome, ADAR copy-number alterations and editase activation have been associated with progression of a broad array of malignancies. In this review we discuss evidence linking aberrant A-to-I editing to cancer and other degenerative diseases, and the mechanisms that may be targeted by novel therapeutic strategies.