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Sirt1-microRNA profile

ABSTRACT: Sirt1, a NAD-dependent deacetylase, has been shown involved in many complex biological functions. We previously demonstrated that Sirt-1 gain of function is neuroprotective in a model of neurodegenenration. We recently found that Sirt1 loss of function (Sirt1Δ mouse) impairs learning, memory, and synaptic plasticity. We used microarray screening to identify potential miRNAs that may be regulated by Sirt1 and ivolved in learning and memory. Total RNA from the hippocampus of SIRT1Δ and control mice was extracted and used for microRNA expression level evaluation.

ORGANISM(S): Mus musculus Rattus norvegicus Human gammaherpesvirus 8 JC polyomavirus Betapolyomavirus macacae Homo sapiens Human immunodeficiency virus 1 Murid gammaherpesvirus 4 Human betaherpesvirus 5 Human alphaherpesvirus 1 Betapolyomavirus hominis human gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE22530 | GEO | 2010/06/24

SECONDARY ACCESSION(S): PRJNA128507

REPOSITORIES: GEO

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Sirt1-microRNA profile

Project description:Sirt1, a NAD-dependent deacetylase, has been shown involved in many complex biological functions. We previously demonstrated that Sirt-1 gain of function is neuroprotective in a model of neurodegenenration. We recently found that Sirt1 loss of function (Sirt1Î mouse) impairs learning, memory, and synaptic plasticity. We used microarray screening to identify potential miRNAs that may be regulated by Sirt1 and ivolved in learning and memory. Total RNA from the hippocampus of SIRT1Î and control mice was extracted and used for microRNA expression level evaluation. Two group experiment, in duplicates. Each sample is compared to a common reference sample, comprised of an equal mixture of all 4 experimental samples.

2010-07-29 | E-GEOD-22530 | biostudies-arrayexpress

NAD+ supplementation limits triple-negative breast cancer metastasis via SIRT1-P66Shc signaling

Project description:NAD+ levels decline with age and in certain disease conditions. NAD+ precursors have been shown to stimulate NAD+ biosynthesis and ameliorate various age-associated diseases in mouse models. However, NAD+ metabolism is complicated in cancer and its role in triple-negative breast cancer (TNBC) remains elusive. Here, we show that NAD+ supplement suppresses tumor metastasis in a TNBC orthotopic patient-derived xenograft (PDX) model. Sirtuin1 lysine deacetylase (SIRT1) is required for the effects since SIRT1 knockdown blocks NAD+-suppressed tumor metastasis. Overexpression of SIRT1 effectively impairs the metastatic potential of TNBC. Importantly, the interaction between SIRT1 and p66Shc causes the deacetylation and functional inactivation of p66Shc, which inhibits epithelial-mesenchymal transition (EMT). Overall, we demonstrate that NAD+ supplementation executes its anti-tumor function via activating the SIRT1-p66Shc axis, which highlights the preventive and therapeutic potential of SIRT1 activators as effective interventions for TNBC.

2023-01-23 | GSE220683 | GEO

Expression analysis upon SIRT1 knockdown in MCF-7 cells

Project description:SIRT1 is a nuclear NAD+-dependent protein deacetylase. Expression microarray analysis was used to study the effect of SIRT1 knockdown on gene expression in MCF-7 breast cancer cells.

2009-05-28 | GSE13459 | GEO

SIRT1 in mouse heart development

Project description:The goal of this project is to investigate the role of SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, in the regulation of heart development. SIRT1 is important for heart development and functions. However, the underlying molecular mechanisms remain undefined. In this study, we analyzed the gene expression profiles in E18.5 WT and SIRT1 KO mouse hearts.

2021-08-23 | GSE86835 | GEO

SIRT1-Dependent Gene Regulation Through Promoter-Directed Recruitment of a Nuclear NAD+ Synthase

Project description:In mammals, nicotinamide phosphoribosyltransferase (NAMPT) and nicotinamide mononucleotide adenylyltransferase 1 (NMNAT-1) constitute a nuclear NAD+ salvage pathway, regulating cellular functions of the NAD+-dependent deacetylase SIRT1. However, little is known about the molecular mechanisms by which NAD+ biosynthesis controls gene transcription in the nucleus. In this study, we show that stable knockdown of NAMPT or NMNAT-1 in MCF-7 breast cancer cells significantly reduced total cellular NAD+ levels. Expression microarray analyses demonstrate that both enzymes have broad and overlapping functions in gene regulation. SIRT1 is a key mediator of NAMPT- and NMNAT-1-dependent gene regulation, and is found at promoters of many of the target genes. Furthermore, SIRT1 deacetylase activity at these promoters is regulated by NAMPT and NMNAT-1. Most significantly, NMNAT-1 interacts with SIRT1 and is recruited to target gene promoters by SIRT1. Our results reveal an unexpected mechanism for the direct control of SIRT1 deacetylase activity at target gene promoters by NMNAT-1. Interactions between NMNAT-1 and SIRT1 at gene promoters may provide a platform for integration of multiple signaling pathways that regulate transcription. This SuperSeries is composed of the SubSeries listed below.

2009-05-28 | GSE13577 | GEO

SIRT1 expression effect on migration and invasion of gastric cancer cells

Project description:Analysis of BGC-823 gastric cancer cells with SIRT1 overexpression or knockdown. SIRT1, a NAD+-dependent protein deacetylase, exerts inhibitory effects on migration and invasion of gastric cancer. Results provide insight into the role of SIRT1 in the metastasis of gastric cancer.

2017-09-07 | GSE103519 | GEO

SIRT1 deficiency enhances RA induced mESC differentiation

Project description:Retinoid homeostasis is critical for normal embryonic development, and both the deficiency and excess of these compounds are associated with congenital malformations. Here we found that SIRT1, the most conserved mammalian NAD+-dependent deacetylase, contributes to the maintenance of homeostatic retinoic acid (RA) signaling and modulates mouse embryonic stem cell (mESC) differentiation. Our data show that SIRT1 deficiency enhances RA signaling, thereby accelerating mES cell differentiation in response to RA. Our findings highlight the importance of SIRT1 in transcriptional regulation of ESC pluripotency and embryogenesis.

2014-08-21 | GSE59140 | GEO

SIRT1 dosage-dependent effects on cell proliferation and metabolism

Project description:The goal of this project is to understand the dosage-dependent effects of SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, on cell proliferation and metabolism. Our recent studies indicate that SIRT1 has a dosage-dependent effect on cell metabolism and proliferation. Heterozygous deletion of SIRT1 enhance glycolysis and glutaminolysis, thereby promoting cell proliferation and stress resistance. Yet homozygous deletion of SIRT1 triggers cellular apoptotic pathways, leading to increased cell death. To understand the molecular mechanisms underlying this dose-dependent effect, we examined the transcriptomes of SIRT1 WT, Het, and KO MEFs cultured in complete DMEM medium by microarray analysis.

2016-12-20 | GSE76088 | GEO

SIRT1 Activation Disrupts Maintenance of Myelodysplastic Syndrome Stem and Progenitor Cells by Restoring TET2 Function [microarray expression profiling]

Project description:Improved understanding of mechanisms regulating myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cell (HSPC) growth and self-renewal is critical for developing MDS therapy. We revealed a novel regulatory axis that SIRT1-deficiency induced TET2 hyperacetylation promotes MDS HSPC functions, and provide an approach to target MDS HSPCs by activating SIRT1 deacetylase. Four Groups: Group1: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for SIRT1); Group2: MDS-L cells transduced with lentiviral vector containing interference squence targeting SIRT1 (SIRT shRNA); Group 3: MDS-L cells transduced with lentiviral vector targeting non-silence squence (control shRNA for TET2); Group 4: MDS-L cells transduced with lentiviral vector containing interference squence targeting TET2 (TET2 shRNA).

2018-08-13 | GSE117272 | GEO

Hepatocyte-specific deletion of SIRT1 alters fatty acid metabolism

Project description:Hepatic metabolic derangements are key components in the development of fatty liver, insulin resistance, and atherosclerosis. SIRT1, a NAD+-dependent protein deacetylase, is an important regulator of energy homeostasis in response to nutrient availability. Here we demonstrate that hepatic SIRT1 regulates fatty acid metabolism by positively regulating PPAR-alpha. Hepatocyte-specific deletion of SIRT1 impairs PPAR-alpha signaling and decreased fatty acid beta-oxidation in the liver. When challenged with a high-fat diet, liver-specific SIRT1 knockout mice develop hepatic steatosis, hepatic inflammation, and endoplasmic reticulum stress. Taken together, our data indicate that SIRT1 plays a vital role in the regulation of hepatic lipid homeostasis.

2009-04-07 | GSE14921 | GEO

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