Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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SIRT1 and H1AcK26 promoter-association in mouse ES cells changes upon oxidative stress


ABSTRACT: Association of the (histone) deacetylase SIRT1 with promoters was assessed to determine putative SIRT1-regulated genes. Based on the observation that the SIRT1 yeast ortholog Sir2 redistributes across the yeast genome in repsonse to genotoxic stress and double strand breaks (DSBs), we investigated the impact of oxidative stress on the chromatin binding pattern of SIRT1. Oxidative stress causes a major change in SIRT1 binding that is accompanied by an inverse H1K26 acetylation pattern. H1K26 was shown to be a direct target for deacetylation by SIRT1. Keywords: ChIP-chip, stress response ES cells were left untreated or treated with 2 mM H2O2 for 1 hour. Both samples were subjected to ChIP against SIRT1, H1AcK26 or rabbit Ig (one IP per treatment and Ab). Input DNA was labeled with Cy3, IP DNA with Cy5, enrichment over input is reported as 2log.

ORGANISM(S): Mus musculus

SUBMITTER: David Sinclair 

PROVIDER: E-GEOD-13075 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


Genomic instability and alterations in gene expression are hallmarks of eukaryotic aging. The yeast histone deacetylase Sir2 silences transcription and stabilizes repetitive DNA, but during aging or in response to a DNA break, the Sir complex relocalizes to sites of genomic instability, resulting in the desilencing of genes that cause sterility, a characteristic of yeast aging. Using embryonic stem cells, we show that mammalian Sir2, SIRT1, represses repetitive DNA and a functionally diverse set  ...[more]

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