Published online 24 February 2005
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Evolutionarily conserved human targets of adenosine to inosine RNA editing
1 Compugen Ltd 72 Pinchas Rosen St, Tel-Aviv 69512, Israel 2 Department of Pediatric Hemato-Oncology, Safra Children's Hospital, Sheba Medical Center and Sackler School of Medicine, Tel Aviv University Tel Aviv, Israel 3 Max F. Perutz Laboratories, Department of Chromosome Biology, University of Vienna Rennweg 14, A-1030 Vienna, Austria 4 Max F. Perutz Laboratories, University Departments at Vienna Biocenter, Institute for Theoretical Chemistry and Molecular Structural Biology, University of Vienna Campus Vienna Biocenter 6/1, Rennweg 95b, A-1030 Vienna, Austria 5 School of Physics and Astronomy, Raymond and Beverly Sackler Faculty of Exact Sciences, Tel Aviv University Tel Aviv 69978, Israel
*To whom correspondence should be addressed at Compugen Ltd., 72 Pinchas Rosen St., Tel-Aviv 69512, Israel. Tel: +972 3 7658503; Fax: +972 3 7658555; Email: erez{at}compugen.co.il
Received December 23, 2004. Accepted January 20, 2005.
A-to-I RNA editing by ADARs is a post-transcriptional mechanism for expanding the proteomic repertoire. Genetic recoding by editing was so far observed for only a few mammalian RNAs that are predominantly expressed in nervous tissues. However, as these editing targets fail to explain the broad and severe phenotypes of ADAR1 knockout mice, additional targets for editing by ADARs were always expected. Using comparative genomics and expressed sequence analysis, we identified and experimentally verified four additional candidate human substrates for ADAR-mediated editing: FLNA, BLCAP, CYFIP2 and IGFBP7. Additionally, editing of three of these substrates was verified in the mouse while two of them were validated in chicken. Interestingly, none of these substrates encodes a receptor protein but two of them are strongly expressed in the CNS and seem important for proper nervous system function. The editing pattern observed suggests that some of the affected proteins might have altered physiological properties leaving the possibility that they can be related to the phenotypes of ADAR1 knockout mice.
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