Z-DNA and Z-RNA in human disease

Communications Biology

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