Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA114267 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE13075: SIRT1 and H1AcK26 promoter-association in mouse ES cells changes upon oxidative stress GSE13120: Age-related gene expression changes in mouse neocortex Refer to individual Series
2010-05-15 | E-GEOD-13121 | biostudies-arrayexpress
Project description: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.
2010-05-15 | E-GEOD-13075 | biostudies-arrayexpress
Project description:Mouse ES cell line transcriptome changes upon replication stress
| PRJNA415135 | ENA
Project description:Mouse ES cell line single cell transcriptome changes upon replication stress
| PRJNA415187 | ENA
Project description: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
2008-11-26 | GSE13075 | GEO
Project description:Gene expression changes upon deletion of CFP1 in mouse ES cells. [mESC_RNAseq]
| PRJNA361071 | ENA
Project description:Chromatin structure affects DNA replication patterns, but the role of specific chromatin modifiers in regulating the replication process is yet unclear. We report that phosphorylation of the human SIRT1 deacetylase on Threonine 530 (T530-pSIRT1) modulates DNA synthesis. T530-pSIRT1 associates with replication origins and inhibits replication from a group of ÒdormantÓ potential replication origins, which initiate replication only when cells are subject to replication stress. Although both active and dormant origins bind T530-pSIRT1, active origins are distinguished from dormant origins by their unique association with an open chromatin mark, histone H3 methylated on lysine 4. SIRT1 phosphorylation also facilitates leading and lagging strand coordination. SIRT1 T530 phosphorylation is essential to prevent DNA breakage upon replication stress and cells harboring SIRT1 that cannot be phosphorylated exhibit a high prevalence of extrachromosomal elements, hallmarks of perturbed replication. These observations suggest that SIRT1 phosphorylation modulates the distribution of replication initiation events to insure genomic stability.
2017-06-02 | GSE94403 | GEO
Project description:Expression data from murine embryonic stem (ES) cells exposed to oxidative stress
| PRJNA121503 | ENA
Project description:A longevity gene, sirtuin 1 (SIRT1) and energy sensor AMP-activated protein kinase (AMPK) have common activators such as caloric restriction, oxidative stress and exercise.The objective is to characterize the role of cardiomyocyte SIRT1 in age-related impaired ischemic AMPK activation and increased susceptibility to ischemic insults.
2017-05-11 | GSE98749 | GEO
Project description:Adipose tissue plays an important role in storing excess nutrients and preventing ectopic lipid accumulation in other organs. Obesity leads to excess lipid storage in adipocytes, resulting in the generation of stress signals and the derangement of metabolic functions. SIRT1 is an important regulatory sensor of nutrient availability in many metabolic tissues. Here we report that SIRT1 functions in adipose tissue to protect from the development of inflammation and obesity under normal feeding conditions, and the progression to metabolic dysfunction under dietary stress. Genetic ablation of SIRT1 from adipose tissue leads to gene expression changes that highly overlap with changes induced by high fat diet in wild type mice, suggesting that dietary stress signals inhibit the activity of SIRT1. Indeed, we show that high fat diet induces the cleavage of SIRT1 in adipose tissue by the inflammation-activated caspase-1, providing a link between dietary stress and predisposition to metabolic dysfunction. Four replicates from four different biological conditions: 1) SIRT1 wild-type fed low fat diet, 2) SIRT1 wild-type fed high fat diet, 3) SIRT1 knock-out fed low fat diet, 4) SIRT1 knock-out fed high fat diet
2012-12-21 | E-GEOD-30247 | biostudies-arrayexpress