dorsal/arxiv
View SchemaEvolutionarily conserved human targets of adenosine to inosine RNA editing
| Authors | Erez Y. Levanon, Martina Hallegger, Yaron Kinar, Ronen Shemesh, Kristina Djinovic-Carugo, Gideon Rechavi, Michael F. Jantsch, Eli Eisenberg |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0502045 |
| URL | https://arxiv.org/abs/q-bio/0502045 |
| DOI | 10.1093/nar/gki239 |
| Journal | Nucleic Acids Research, Vol. 33, 1162-1168 (2005) |
Abstract
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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"abstract": "A-to-I RNA editing by ADARs is a post-transcriptional mechanism for expanding\nthe proteomic repertoire. Genetic recoding by editing was so far observed for\nonly a few mammalian RNAs that are predominantly expressed in nervous tissues.\nHowever, as these editing targets fail to explain the broad and severe\nphenotypes of ADAR1 knockout mice, additional targets for editing by ADARs were\nalways expected. Using comparative genomics and expressed sequence analysis, we\nidentified and experimentally verified four additional candidate human\nsubstrates for ADAR-mediated editing: FLNA, BLCAP, CYFIP2 and IGFBP7.\nAdditionally, editing of three of these substrates was verified in the mouse\nwhile two of them were validated in chicken. Interestingly, none of these\nsubstrates encodes a receptor protein but two of them are strongly expressed in\nthe CNS and seem important for proper nervous system function. The editing\npattern observed suggests that some of the affected proteins might have altered\nphysiological properties leaving the possibility that they can be related to\nthe phenotypes of ADAR1 knockout mice.",
"arxiv_id": "q-bio/0502045",
"authors": [
"Erez Y. Levanon",
"Martina Hallegger",
"Yaron Kinar",
"Ronen Shemesh",
"Kristina Djinovic-Carugo",
"Gideon Rechavi",
"Michael F. Jantsch",
"Eli Eisenberg"
],
"categories": [
"q-bio.GN"
],
"doi": "10.1093/nar/gki239",
"journal_ref": "Nucleic Acids Research, Vol. 33, 1162-1168 (2005)",
"title": "Evolutionarily conserved human targets of adenosine to inosine RNA editing",
"url": "https://arxiv.org/abs/q-bio/0502045"
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