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AbstractAbstract
[en] Sir2 maintains genomic stability in multiple ways in yeast. As a NAD+-dependent histone deacetylase, Sir2 has been reported to control chromatin silencing. In both budding yeast and Drosophila, overexpression of Sir2 extends life span. Previous reports have also demonstrated that Sir2 participate at DNA damage repair. A protein complex containing Sir2 has been reported to translocate to DNA double-strand breaks. Following DNA damage response, SIRT1 deacetylates p53 protein and attenuates its ability as a transcription factor. Consequently, SIRT1 over-expression increases cell survival under DNA damage inducing conditions. These previous observations mean a possibility that signals generated during the process of DNA repair are delivered through SIRT1 to acetylated p53. We present herein functional evidence for the involvement of SIRT1 in DNA repair response to radiation. In addition, this modulation of DNA repair activity may be connected to deacetylation of MRN proteins
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Korean Nuclear Society, Daejeon (Korea, Republic of); [1 CD-ROM]; May 2009; [2 p.]; 2009 spring meeting of the KNS; Jeju (Korea, Republic of); 18-23 May 2009; Available from KNS, Daejeon (KR); 3 refs, 1 fig
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Miscellaneous
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Conference
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