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dc.contributor.authorHegde, M.L.
dc.contributor.authorDutta, A.
dc.contributor.authorYang, C.
dc.contributor.authorMantha, Anil K.
dc.contributor.authorHegde, P.M.
dc.contributor.authorPandey, A.
dc.contributor.authorSengupta, S.
dc.contributor.authorYu, Y.
dc.contributor.authorCalsou, P.
dc.contributor.authorChen, D.
dc.contributor.authorLees-Miller, S.P.
dc.contributor.authorMitra, S.
dc.date.accessioned2013-01-11T14:57:34Z
dc.date.available2013-01-11T14:57:34Z
dc.date.issued2016
dc.date.issued2016
dc.identifier.citationHegde, M. L., Dutta, A., Yang, C., Mantha, A. K., Hegde, P. M., Pandey, A., . . . Mitra, S. (2016). Scaffold attachment factor A (SAF-A) and Ku temporally regulate repair of radiation-induced clustered genome lesions. Oncotarget, 7(34), 54430-54444. doi: 10.18632/oncotarget.9914en_US
dc.identifier.issnOnline- 1949-2553
dc.identifier.issn19492553
dc.identifier.urihttp://kr.cup.edu.in/handle/32116/381
dc.description.abstractIonizing radiation (IR) induces highly cytotoxic double-strand breaks (DSBs) and also clustered oxidized bases in mammalian genomes. Base excision repair (BER) of bi-stranded oxidized bases could generate additional DSBs as repair intermediates in the vicinity of direct DSBs, leading to loss of DNA fragments. This could be avoided if DSB repair via DNA-PK-mediated nonhomologous end joining (NHEJ) precedes BER initiated by NEIL1 and other DNA glycosylases (DGs). Here we show that DNAPK subunit Ku inhibits DGs via direct interaction. The scaffold attachment factor (SAF)-A, (also called hnRNP-U), phosphorylated at Ser59 by DNA-PK early after IR treatment, is linked to transient release of chromatin-bound NEIL1, thus preventing BER. SAF-A is subsequently dephosphorylated. Ku inhibition of DGs in vitro is relieved by unphosphorylated SAF-A, but not by the phosphomimetic Asp59 mutant. We thus propose that SAF-A, in concert with Ku, temporally regulates base damage repair in irradiated cell genome.en_US
dc.language.isoenen_US
dc.publisherImpact Journals LLCen_US
dc.titleScaffold attachment factor A (SAF-A) and Ku temporally regulate repair of radiation-induced clustered genome lesionsen_US
dc.typeArticleen_US
dc.identifier.doi10.18632/oncotarget.9914
dc.identifier.urlhttp://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=9914&path[]=31123
dc.title.journalOncotarget


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