Genetic variants that down-regulate a specific form of post-transcriptional RNA editing could be an important potential mechanism underlying common inflammatory diseases.
A paper recently published in Nature outlined how researchers from Stanford University, California identified genetic variants that affected RNA editing from the genomic data of 838 human deceased donors from the Genotype-Tissue Expression catalogue. Further analysis looked at whether these variants were on parts of the genome previously associated with inflammatory diseases such as lupus, multiple sclerosis and coronary artery disease.
The variants they had identified had stronger associations with inflammatory diseases compared to variants affecting gene expression or splicing, which have previously been linked with those conditions.
