Mouse models to elucidate the functional roles of adenosine-to-inosine editing.
The conversion of adenosine to inosine (A-to-I) by RNA editing is a widespread RNA processing event by which genomically encoded sequences are altered through site-specific deamination of adenosine residue(s) in RNA transcripts through the actions of a family of double-stranded RNA-specific adenosine deaminases (ADARs). While significant advances have been made regarding the functional consequences of A-to-I editing using heterologous expression systems, the physiological relevance of such RNA modifications in mammals has been addressed effectively using gene-targeting strategies in mice via homologous recombination in embryonic stem (ES) cells. These gene-targeting approaches have allowed the generation of mutant mouse strains in which site-specific editing events can be fixed in the fully edited or nonedited state for individual ADAR targets, expression of ADAR proteins can be selectively ablated, or a combination of ADAR elimination and ADAR target modification can be used for a more in-depth understanding of the biological consequences of A-to-I editing dysregulation.
Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Elizabeth Y
EY
Rula
Ronald B
RB
Emeson
D000241:Adenosine / Q000737:chemistry*; D000818:Animals; D001483:Base Sequence; D007288:Inosine / Q000737:chemistry*; D007473:Ion Channels / Q000737:chemistry; D051379:Mice; D008822:Mice, Transgenic; D008969:Molecular Sequence Data; D009154:Mutation; D009690:Nucleic Acid Conformation; D015221:Potassium Channels / Q000737:chemistry; D017434:Protein Structure, Tertiary; D017393:RNA Editing / Q000235:genetics*; D044405:Receptor, Serotonin, 5-HT2C / Q000737:chemistry; D013379:Substrate Specificity
D007473:Ion Channels; D015221:Potassium Channels; D044405:Receptor, Serotonin, 5-HT2C; D007288:Inosine; D000241:Adenosine