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dc.contributor.authorStratton, M
dc.date.accessioned2018-06-11T13:42:01Z
dc.date.issued2004-12
dc.identifier12
dc.identifier.citationGENOME RESEARCH, 2004, 14 pp. 2379 - 2387
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1826
dc.description.abstractA survey of RNA editing in human brain We have conducted a survey of RNA editing in human brain by comparing sequences of clones from a human brain cDNA library to the reference human genome sequence and to genomic DNA from the same individual. In the RNA sample from which the library was constructed, -1:2000 nucleotides were edited out of \ensuremath>3 Mb surveyed. All edits were adenosine to inosine (A–\ensuremath>I) and were predominantly in intronic and in intergenic RNAs. No edits were found in translated exons and few in untranslated exons. Most edits were in high-copy-number repeats, usually Alus. Analysis of the genome in the vicinity of edited sequences strongly supports the idea that formation of intramolecular double- stranded RNA with an inverted copy underlies most A–\ensuremath>I editing. The likelihood of editing is increased by the presence of two inverted copies of a sequence within the same intron, proximity of the two sequences to each other (preferably within 2 kb), and by a high density of inverted copies in the vicinity. Editing exhibits sequence preferences and is less likely at an adenosine 3’ to a guanosine and more likely at an adenosine 5 to a guanosine. Simulation by BLAST alignment of the double-stranded RNA molecules that underlie known edits indicates that there is a greater likelihood of A–\ensuremath>I editing at A:C mismatches than editing at other mismatches or at A:U matches. However, because A:U matches in double-stranded RNA are more common than all mismatches, overall the likely effect of editing is to increase the number of mismatches in double- stranded RNA.
dc.format.extent2379 - 2387
dc.languageeng
dc.language.isoeng
dc.titleA survey of RNA editing in human brain
dc.typeJournal Article
rioxxterms.licenseref.startdate2004-12
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfGENOME RESEARCH
pubs.noteskeywords: Adenosine deaminases; kainate receptor; messenger-rna; adar2; mechanisms; conversion; abundant; mutants; protein; sites
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Genetic Susceptibility
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Genetic Susceptibility
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Genetic Susceptibility
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Genetics and Epidemiology/Genetic Susceptibility
pubs.volume14
pubs.embargo.termsNot known
icr.researchteamGenetic Susceptibilityen_US
dc.contributor.icrauthorStratton, Michaelen


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