TY - JOUR
T1 - Evolutionarily conserved human targets of adenosine to inosine RNA editing
AU - Levanon, Erez Y.
AU - Hallegger, Eva-Martina
AU - Kinar, Yaron
AU - Shemesh, Ronen
AU - Djinovic-Carugo, Kristina
AU - Rechavi, Gideon
AU - Jantsch, Franz-Michael
AU - Eisenberg, Eli
AU - Thalhammer, Ursula
N1 - DOI: 10.1093/nar/gki239
Coden: NARHA
Affiliations: Compugen Ltd., 72 Pinchas Rosen St., Tel-Aviv 69512, Israel; Department of Pediatric Hemato-Oncology, Safra Children's Hospital, Tel Aviv University, Tel Aviv, Israel; Max F. Perutz Laboratories, Department of Chromosome Biology, University of Vienna, Rennweg 14, A-1030 Vienna, Austria; Max F. Perutz Laboratories, Institute for Theoretical Chemistry and Molecular Structural Biology, University of Vienna, Campus Vienna Biocenter 6/1, A-1030 Vienna, Austria; School of Physics and Astronomy, Raymond and Beverly Sackler Faculty of Exact Sciences, Tel Aviv University, Tel Aviv 69978, Israel
Adressen: Levanon, E.Y.; Compugen Ltd.; 72 Pinchas Rosen St. Tel-Aviv 69512, Israel; email: [email protected]
Source-File: MFPLUniWienScopus.csv
Import aus Scopus: 2-s2.0-14844348294
Importdatum: 07.12.2006 15:11:40
15.01.2009: Datenanforderung 2651 (Import Sachbearbeiter)
09.02.2010: Datenanforderung UNIVIS-DATEN-DAT.RA-2 (Import Sachbearbeiter)
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. Œ The Author 2005. Published by Oxford University Press. All rights reserved.
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. Œ The Author 2005. Published by Oxford University Press. All rights reserved.
U2 - 10.1093/nar/gki239
DO - 10.1093/nar/gki239
M3 - Article
SN - 0305-1048
VL - 33
SP - 1162
EP - 1168
JO - Nucleic Acids Research
JF - Nucleic Acids Research
IS - 4
ER -