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Article: Double-stranded break can be repaired by single-stranded oligonucleotides via the ATM/ATR pathway in mammalian cells

TitleDouble-stranded break can be repaired by single-stranded oligonucleotides via the ATM/ATR pathway in mammalian cells
Authors
Issue Date2008
PublisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/ard
Citation
Oligonucleotides, 2008, v. 18 n. 1, p. 21-32 How to Cite?
AbstractSingle-stranded oligonucleotide (SSO)-mediated gene modification is a newly developed tool for site-specific gene repair in mammalian cells; however, the corrected cells always show G2/M arrest and cannot divide to form colonies. This phenomenon and the unclear mechanism seriously challenge the future application of this technique. In this study, we developed an efficient SSO-mediated DNA repair system based on double-stranded break (DSB) induction. We generated a mutant EGFP gene with insertions of 24 bp to 1.6 kb in length as a reporter integrated in mammalian cell lines. SSOs were successfully used to delete the insertion fragments upon DSB induction at a site near the insertion. We demonstrated that this process is dependent on the ATM/ATR pathway. Importantly, repaired cell clones were viable. Effects of deletion length, SSO length, strand bias, and SSO modification on gene repair frequency were also investigated. © 2008 Mary Ann Liebert, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/147580
ISSN
2013 Impact Factor: 3.077
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Zen_US
dc.contributor.authorZhou, ZJen_US
dc.contributor.authorLiu, DPen_US
dc.contributor.authorHuang, JDen_US
dc.date.accessioned2012-05-29T06:04:45Z-
dc.date.available2012-05-29T06:04:45Z-
dc.date.issued2008en_US
dc.identifier.citationOligonucleotides, 2008, v. 18 n. 1, p. 21-32en_US
dc.identifier.issn1545-4576en_US
dc.identifier.urihttp://hdl.handle.net/10722/147580-
dc.description.abstractSingle-stranded oligonucleotide (SSO)-mediated gene modification is a newly developed tool for site-specific gene repair in mammalian cells; however, the corrected cells always show G2/M arrest and cannot divide to form colonies. This phenomenon and the unclear mechanism seriously challenge the future application of this technique. In this study, we developed an efficient SSO-mediated DNA repair system based on double-stranded break (DSB) induction. We generated a mutant EGFP gene with insertions of 24 bp to 1.6 kb in length as a reporter integrated in mammalian cell lines. SSOs were successfully used to delete the insertion fragments upon DSB induction at a site near the insertion. We demonstrated that this process is dependent on the ATM/ATR pathway. Importantly, repaired cell clones were viable. Effects of deletion length, SSO length, strand bias, and SSO modification on gene repair frequency were also investigated. © 2008 Mary Ann Liebert, Inc.en_US
dc.languageengen_US
dc.publisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/arden_US
dc.relation.ispartofOligonucleotidesen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThis is a copy of an article published in the [Oligonucleotides] © [2008] [copyright Mary Ann Liebert, Inc.]; [Oligonucleotides] is available-
dc.subject.meshAllelesen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCell Cycle Proteins - Metabolismen_US
dc.subject.meshCell Lineen_US
dc.subject.meshDna Damageen_US
dc.subject.meshDna Primersen_US
dc.subject.meshDna Repairen_US
dc.subject.meshDna-Binding Proteins - Metabolismen_US
dc.subject.meshFlow Cytometryen_US
dc.subject.meshHumansen_US
dc.subject.meshOligonucleotides - Metabolismen_US
dc.subject.meshProtein-Serine-Threonine Kinases - Metabolismen_US
dc.subject.meshRna, Small Interferingen_US
dc.subject.meshTumor Suppressor Proteins - Metabolismen_US
dc.titleDouble-stranded break can be repaired by single-stranded oligonucleotides via the ATM/ATR pathway in mammalian cellsen_US
dc.typeArticleen_US
dc.identifier.emailZhou, ZJ:zhongjun@hkucc.hku.hken_US
dc.identifier.emailHuang, JD:jdhuang@hkucc.hku.hken_US
dc.identifier.authorityZhou, ZJ=rp00503en_US
dc.identifier.authorityHuang, JD=rp00451en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1089/oli.2007.0093en_US
dc.identifier.pmid18321160en_US
dc.identifier.scopuseid_2-s2.0-44449089576en_US
dc.identifier.hkuros146694-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44449089576&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume18en_US
dc.identifier.issue1en_US
dc.identifier.spage21en_US
dc.identifier.epage32en_US
dc.identifier.isiWOS:000254308100003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, Z=7410048523en_US
dc.identifier.scopusauthoridZhou, ZJ=8631856300en_US
dc.identifier.scopusauthoridLiu, DP=21934191400en_US
dc.identifier.scopusauthoridHuang, JD=8108660600en_US

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