Disease relevance of Adarb1

• The mammalian RNA-specific adenosine deaminases DRADA/dsRAD (alias ADAR) and RED1 (alias ADARB1) have been implicated in the site-selective editing of brain-expressed pre-mRNAs for glutamate receptor subunits and of antigenomic RNA of hepatitis delta virus [1].

High impact information on Adarb1

• RED2 further differs from RED1 in having a 54-residue amino-terminal extension which includes an arginine-rich motif [1].
• RED2 is closely sequence-related to RED1 but appears to be expressed only in the brain, where expression is widespread reaching highest levels in olfactory bulb and thalamus [1].
• Co-transfection of a vector expressing either NF1-L or NF1/Red1 repressed the transcription of the PKL enhancer unit-chloramphenicol acetyltransferase (CAT) fusion gene in HepG2 cells, whereas co-transfection of a vector expressing HNF4 activated the transcription of the same reporter gene [2].
• In addition, we found that the adenosine deaminases, DRADA, RED1 and RED2, which edit ionotropic glutamate receptors in the brain, are expressed in the adult optic nerve and in oligodendrocytes, the major cell type in this structure [3].
• Finally, cerebellar granule cells express a previously unreported variant of RED1 which appears to arise from developmentally regulated alternative splicing [4].

Analytical, diagnostic and therapeutic context of Adarb1

• Peptide sequence analysis revealed that these proteins were nuclear factor (NF) 1-L and NF1/Red1 [2].

References