RNA editing underlies genetic risk of common inflammatory diseases.

ABSTRACT: A major challenge in human genetics is to identify the molecular mechanisms of trait-associated and disease-associated variants. To achieve this, quantitative trait locus (QTL) mapping of genetic variants with intermediate molecular phenotypes such as gene expression and splicing have been widely adopted^1,2. However, despite successes, the molecular basis for a considerable fraction of trait-associated and disease-associated variants remains unclear^3,4. Here we show that ADAR-mediated adenosine-to-inosine RNA editing, a post-transcriptional event vital for suppressing cellular double-stranded RNA (dsRNA)-mediated innate immune interferon responses^5-11, is an important potential mechanism underlying genetic variants associated with common inflammatory diseas

SUBMITTER: Li Q 

PROVIDER: S-EPMC9790998 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature