ADARB1 ELISA Kit

Adenosine deaminases that act on RNA bind double-stranded and structured RNAs and convert adenosines to inosines by hydrolytic deamination. Inosines are recognized as guanosines, and, hence, RNA editing alters the sequence information but also structure of RNAs. Editing by ADARs is widespread and essential for normal life and development. Precursors of miRNAs are abundantly edited by ADARs, but neither the abundance nor the consequences of miRNA editing has been firmly established. Using transgenic mouse embryos that are deficient in the two enzymatically active editing enzymes ADAR and ADARB1, we compare relative frequencies but also sequence composition of miRNAs in these genetically modified backgrounds to wild-type mice by "next-generation sequencing." Deficiency of ADARB1 leads to a reproducible change in abundance of specific miRNAs and their predicted targets. Changes in miRNA abundance seem unrelated to editing events. Additional deletion of ADAR has surprisingly little impact on the mature miRNA repertoire, indicating that miRNA expression is primarily dependent on ADARB1. A-to-G transitions reflecting A-to-I editing events can be detected at few sites and at low frequency during the early embryonic stage investigated. Again, most editing events are ADARB1-dependent with only few editing sites being specifically edited by ADAR. Besides known editing events in miRNAs, a few novel, previously unknown editing events were identified. Some editing events are located to the seed region of miRNAs, opening the possibility that editing leads to their retargeting.

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.