This gene encodes a double-stranded-RNA-specific adenosine deaminase that is involved in editing pre-mRNAs by site-specific conversion of adenosine (A) to inosine (I). Substrates for this enzyme include ionotropic glutamate receptors (GluR2-6) and serotonin receptor (5HT2C). Studies in rodents have shown that this protein can modify its own pre-mRNA by A->I editing to create a novel acceptor splice site, alternative splicing to which results in down regulation of its protein expression. Additional splicing events result in transcript variants encoding different isoforms.
Pathway
C6 deamination of adenosine; Gene Expression; mRNA Editing: A to I Conversion.
Citations
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References
Spatio-temporal profiling of Filamin A RNA-editing reveals ADAR preferences and high editing levels outside neuronal tissues
RNA editing by ADARs can change the coding potential of protein-coding mRNAs. So far, this type of RNA editing has mainly been shown to affect RNAs expressed in the nervous system with much lower editing levels being observed in other tissues. The actin crosslinking proteins filamin and filamin are widely expressed in most tissues. The mRNAs encoding either protein are edited at the same position leading to a conserved Q to R exchange in both proteins. Using bar-coded next generation sequencing, we show that editing of filamin is most abundant in the gastrointestinal tract and only to a lesser extent in the nervous system. Using knockout mice, we show that ADARB1 (ADAR2) is responsible for the majority of FLNA editing, while ADAR1 can edit filamin mRNA in some tissues quite efficiently. Interestingly, editing levels of filamin and do not follow the same trend across tissues, suggesting a substrate-specific regulation of editing.
Screening of chromosomal region 21q22.3 for mutations in genes associated with neuronal Ca2+ signalling in bipolar affective disorder
ACTA BIOCHIMICA POLONICA
Authors: Kostyrko, Andrzej; Hauser, Joanna; Rybakowski, Janusz K.; Trzeciak, Wieslaw H.
The therapeutic effect of lithium in bipolar affective disorder may be connected with decreasing intracellular Ca2+ concentrations. Several linkage studies have identified a potential bipolar affective disorder susceptibility locus within chromosomal region 21q22.3. This locus contains two genes expressed in the brain - ADARB1 and TRPM2 - involved in regulating intracellular Ca2+ concentrations. The aim of this study was an identification of mutations in the coding sequences of ADARB1 and TRPM2 and their association with bipolar affective disorder. For that purpose we screened 60 patients with bipolar affective disorder and a control group of 66 subjects using single strand conformation polymorphism and sequence analysis. For rapid screening we performed restriction fragment length polymorphism analysis. Screening of bipolar affective disorder patients for mutations in TRPM2 led to identification of three novel and four known transitions. Two transitions resulted in the substitutions: R755C and A890V. Screening of the coding sequence of ADARB1 did not reveal any mutations except one already known transition. A comparison of the transition frequency in patients and controls does not support association of the detected mutations with bipolar affective disorder. According to our results, bipolar affective disorder may not be caused by mutations in ADARB1. However, this study does not exclude TRPM2 as a candidate gene since we have screened only about 30 per cent of the entire coding sequence of this large gene.
COA
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