کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2838472 | 1165015 | 2015 | 11 صفحه PDF | دانلود رایگان |

• A-to-I editing increases transcriptome diversity through multiple mechanisms.
• Aberrant regulation of A-to-I editing promotes cancer and degenerative disease.
• The functional impact of many RNA editing sites is still not fully understood.
• Treatments reverting A-to-I editing may have great potential in several diseases.
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.
Journal: - Volume 21, Issue 9, September 2015, Pages 549–559