Practice question

Adenosine to inosine editing, most frequent editing in mammalian transcriptomes, catalyzed by ADAR family adenosine deaminases acting on RNA containing double-stranded regions. Enzymes ADAR1 p110 p150 and ADAR2 deaminate adenosine at C6 position via hydrolytic deamination producing inosine, which ribosome and spliceosome read as guanosine due to base pairing with cytidine. Targets include glutamate receptor GluA2 Q/R site altering calcium permeability, serotonin 5HT2C receptor fine-tuning signaling. ADARs contain dsRNA binding domains, deaminase domain, editing complementary sequences often within Alu repeats. Deficiency triggers MDA5-mediated interferon response.