Publication:
Alu siRNA to increase Alu element methylation and prevent DNA damage

dc.contributor.authorMaturada Patchsungen_US
dc.contributor.authorSirapat Settayanonen_US
dc.contributor.authorMonnat Pongpanichen_US
dc.contributor.authorDharm Mutiranguraen_US
dc.contributor.authorPornrutsami Jintarithen_US
dc.contributor.authorApiwat Mutiranguraen_US
dc.contributor.otherChulalongkorn Universityen_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2019-08-23T10:37:36Z
dc.date.available2019-08-23T10:37:36Z
dc.date.issued2018-02-01en_US
dc.description.abstract© 2018 Apiwat Mutirangura. Global DNA hypomethylation promoting genomic instability leads to cancer and deterioration of human health with age. Aim: To invent a biotechnology that can reprogram this process. Methods: We used Alu siRNA to direct Alu interspersed repetitive sequences methylation in human cells. We evaluated the correlation between DNA damage and Alu methylation levels. Results: We observed an inverse correlation between Alu element methylation and endogenous DNA damage in white blood cells. Cells transfected with Alu siRNA exhibited high Alu methylation levels, increased proliferation, reduced endogenous DNA damage and improved resistance to DNA damaging agents. Conclusion: Alu methylation stabilizes the genome by preventing accumulation of DNA damage. Alu siRNA could be useful for evaluating reprograming of the global hypomethylation phenotype in cancer and aging cells.en_US
dc.identifier.citationEpigenomics. Vol.10, No.2 (2018), 175-185en_US
dc.identifier.doi10.2217/epi-2017-0096en_US
dc.identifier.issn1750192Xen_US
dc.identifier.issn17501911en_US
dc.identifier.other2-s2.0-85041118554en_US
dc.identifier.urihttps://repository.li.mahidol.ac.th/handle/20.500.14594/45252
dc.rightsMahidol Universityen_US
dc.rights.holderSCOPUSen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85041118554&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleAlu siRNA to increase Alu element methylation and prevent DNA damageen_US
dc.typeArticleen_US
dspace.entity.typePublication
mu.datasource.scopushttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85041118554&origin=inwarden_US

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