TY - JOUR
T1 - Evolutionarily conserved human targets of adenosine to inosine RNA editing
AU - Levanon, Erez Y.
AU - Hallegger, Martina
AU - Kinar, Yaron
AU - Shemesh, Ronen
AU - Djinovic-Carugo, Kristina
AU - Rechavi, Gideon
AU - Jantsch, Michael F.
AU - Eisenberg, Eli
N1 - Funding Information:
We thank Rotem Sorek for his useful suggestions and comments on this work, and Shulamit Michaeli for helpful discussion. The work of E.Y.L. was done in partial fulfilment of the requirements for a PhD degree from the Sackler Faculty of Medicine, Tel Aviv University, Israel. Part of this work was supported by the Austrian Science Foundation grant SFB1706 to M.F.J. Funding to pay the Open Access publication charges for this article was provided by Compugen Ltd.
PY - 2005
Y1 - 2005
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=14844348294&partnerID=8YFLogxK
U2 - 10.1093/nar/gki239
DO - 10.1093/nar/gki239
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AN - SCOPUS:14844348294
SN - 0305-1048
VL - 33
SP - 1162
EP - 1168
JO - Nucleic Acids Research
JF - Nucleic Acids Research
IS - 4
ER -
