期刊论文详细信息
Communications Biology | |
Z-DNA and Z-RNA in human disease | |
Alan Herbert1  | |
[1]Discovery, InsideOutBio, Charlestown, USA | |
DOI : 10.1038/s42003-018-0237-x | |
学科分类:生物科学(综合) | |
来源: Nature Publishing Group | |
【 摘 要 】
Left-handed Z-DNA/Z-RNA is bound with high affinity by the Zα domain protein family that includes ADAR (a double-stranded RNA editing enzyme), ZBP1 and viral orthologs regulating innate immunity. Loss-of-function mutations in ADAR p150 allow persistent activation of the interferon system by Alu dsRNAs and are causal for Aicardi-Goutières Syndrome. Heterodimers of ADAR and DICER1 regulate the switch from RNA- to protein-centric immunity. Loss of DICER1 function produces age-related macular degeneration, a different type of Alu-mediated disease. The overlap of Z-forming sites with those for the signal recognition particle likely limits invasion of primate genomes by Alu retrotransposons.【 授权许可】
CC BY
【 预 览 】
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RO201904024472511ZK.pdf | 1654KB | download |