Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Sirt2 deletion in mouse hepatocytes on gene experession in mouse livers overexpressed with GFP or MET/CAT

ABSTRACT: Effect of Sirt2 deletion in mouse hepatocytes on gene experession in mouse livers overexpressed with GFP or MET/CAT

PROVIDER: PRJNA1178649 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Effect of Sirt2 deletion in mouse hepatocytes on gene experession in mouse livers overexpressed with GFP or MET/CAT

Project description:There is a gap in our understanding of mechanisms promoting hepatocellular carcinoma (HCC), and this limits our ability to provide targeted therapy interventions for HCC. In HCC samples, NAD-dependent deacetylase sirtuin 2 (SIRT2) levels are increased and associated with a significantly worse prognosis, but the role of SIRT2 in hepatocarcinInogenesis remains controversial. In this study, we investigated the role of SIRT2 in HCC development and examined the effect of Sirt2 deletion in hepatocytes on gene expression in mouse livers overexpressed with GFP control or MET/CAT.

2025-07-23 | GSE280462 | GEO

Gene expression profiling of mouse liver cells treated with or without MET/CAT and SB transposase

Project description:mice were induced with MET/CAT and SB for 0, 2 or 7 weeks , then mRNA were extracted for high-throughput sequencing

2020-07-29 | GSE155284 | GEO

Gene expression profiling of mouse liver cells treated with or without MET/CAT and SB transposase

Project description:Gene expression profiling of mouse liver cells treated with or without MET/CAT and SB transposase

| PRJNA649242 | ENA

Next Generation Sequencing of β-cat lox(ex3) (Ctrl) mouse and β-cat lox(ex3);Nex-Cre (β-cat overexpression, β-cat Ovp) mouse Transcriptomes

Project description:Using RNA-seq to sequence the transcriptomes of β-cat lox(ex3) (Ctrl) and β-cat lox(ex3);Nex-Cre (β-cat Ovp) mice, we did not find significant change in the expression level of classical Wnt target genes.

2017-09-02 | GSE95629 | GEO

The deacetylase SIRT2 contributes to autoimmune disease pathogenesis by modulating IL-17A and IL-2 transcription

Project description:Aberrant expression of IL-17A together with abated IL-2 production by effector CD4+ T cells contributes to the pathogenesis of systemic lupus erythematosus (SLE). Here we report that Sirtuin 2 (SIRT2), a member of the family of NAD+-dependent histone deacetylases, suppresses IL-2 production by CD4+ T cells while it promotes their differentiation into Th17 cells. Mechanistically, we show that SIRT2 is responsible for the deacetylation of p70S6K and the activation of the mTORC1/HIF-1α/RORγt pathway and the generation of Th17 cells differentiation. Additionally, SIRT2 is responsible for the deacetylation of c-Jun and histones on the Il-2 gene, resulting in decreased IL-2 production. We found that the transcription factor inducible cAMP early repressor (ICER), which is overexpressed in T cells from people with SLE and lupus-prone mice, binds directly to the Sirt2 promoter and promotes its transcription. AK-7, a SIRT2 inhibitor limited the ability of adoptively transferred antigen-specific CD4+ T cells to cause autoimmune encephalomyelitis and disease in the lupus-prone MRL/lpr mice. Finally, CD4+ T cells from SLE patients exhibited increased expression of SIRT2, and pharmacological inhibition of SIRT2 in primary CD4+ T cells from patients with SLE attenuated their ability to differentiate into Th17 cells and promoted IL-2–producing T cells. Collectively, these results suggest that SIRT2-mediated deacetylation is essential for the aberrant expression of IL-17A and IL-2 and that SIRT2 may be a promising molecular target for new therapies for SLE.

2022-03-30 | GSE199496 | GEO

Impact of Sirt2 deficiency on downstream TCR signaling in mouse melanoma tumor-infiltrating T lymphocytes

Project description:The T-cell receptor (TCR) signaling pathway is a highly regulated system designed to prevent autoimmunity while ensuring effective immune responses. This regulation is typically mediated through phosphorylation, dephosphorylation, and ubiquitination. Sirt2, is a cytoplasmic NAD+-dependent histone deacetylase with anti-aging and antioxidant properties. Here we reveal acetylation modulated by Sirt2 as a previously unrecognized process controlling TCR signaling. In our study, we found that the loss of Sirt2 in T cells leads to enhanced TCR signaling following T cell activation. Furthermore, we demonstrated that inhibiting Sirt2 in both murine and human tumor-infiltrating lymphocytes restores TCR responsiveness and enhances their anti-tumor activity. This suggests Sirt2 targeting as a potential therapeutic approach for reactivating exhausted T cells within the tumor microenvironment.

2025-10-15 | GSE265880 | GEO

transcriptome analysis of SIRT2 dependent genes modulated during infection by Listeria monocytogenes

Project description:tissue culture cells were treated with an inhibitor to the deacetylase SIRT2 (AGK2) and infected with Listeria monocytogenes

2013-06-01 | E-MEXP-3912 | biostudies-arrayexpress

Metabolic control of adaptive b-cell proliferation by the protein deacetylase SIRT2

Project description:Selective and controlled expansion of endogenous b-cells has been pursued as a potential therapy for diabetes. Ideally, such therapies would preserve feedback control of b-cell proliferation to avoid excessive b-cell expansion and an increased risk of hypoglycemia. Here, we identified a regulator of b-cell proliferation whose inactivation results in controlled b-cell expansion: the protein deacetylase Sirtuin 2 (SIRT2). Sirt2 deletion in b-cells of mice increased b-cell proliferation during hyperglycemia with little effect in homeostatic conditions, indicating preservation of feedback control of b-cell mass. SIRT2 restrains proliferation of human islet b-cells cultured in glucose concentrations above the glycemic set point, demonstrating conserved SIRT2 function. Analysis of acetylated proteins in islets treated with a SIRT2 inhibitor revealed that SIRT2 deacetylates enzymes involved in oxidative phosphorylation, dampening the adaptive increase in oxygen consumption during hyperglycemia. At the transcriptomic level, Sirt2 inactivation has context-dependent effects on b-cells, with Sirt2 controlling how b-cells interpret hyperglycemia as a stress. Finally, we provide proof-of-principle that systemic administration of a GLP1-coupled Sirt2-targeting antisense oligonucleotide achieves b-cell selective Sirt2 inactivation and stimulates b-cell proliferation under hyperglycemic conditions. Overall, these studies identify a therapeutic strategy for increasing b-cell mass in diabetes without circumventing feedback control of b-cell proliferation.

2025-07-17 | GSE252859 | GEO

Essential Role of Sirt2 in Type I Interferon Signaling

Project description:We provide evidence for the essential role of Sirt2 in IFN mediated signaling. Our studies demonstrate that SIRT2 controls expression of key interferon stimulated genes (ISGs) that mediate important biological functions, including anti-viral and antineoplastic responses.

2015-12-31 | GSE66033 | GEO

Sirt2 Inhibition Reprograms T Cell Metabolism to Confer Superior Anti-Tumor Immunity

Project description:Metabolism is a key driver of T cell functions, and the switch from oxidative-phosphorylation to aerobic glycolysis is a hallmark of T cell activation. However, the mechanisms underlying the metabolic switch remain unclear. Here, we report that the Sirtuin-2 (Sirt2) deacetylase protein functions as a metabolic checkpoint that harnesses T cell effector functions and impairs anti-tumor immunity. Specifically, upregulation of Sirt2 expression in human tumor-infiltrating T lymphocytes (TILs) negatively correlates with response to Nivolumab and TIL therapy in non-small cell lung cancer. Mechanistically, Sirt2 suppresses aerobic glycolysis by deacetylating key glycolytic enzymes. Accordingly, Sirt2-deficient T cells manifest increased glycolysis, display enhanced proliferation and effector functions, and have superior anti-tumor activity. Importantly, pharmacologic inhibition of Sirt2 endows human TILs with these superior metabolic fitness and enhanced effector functions. These findings indicate Sirt2 as an actionable target for reprogramming T cell metabolism to augment a broad spectrum of cancer immunotherapies.

2020-09-16 | GSE151421 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data