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Mus musculus

ABSTRACT: RNA-seq transcriptome analysis in naïve and TNF-a-treated Sirt6-silenced YAMC cells to enrich for direct Sirt6 targets associated with inflammatory stimulation.

PROVIDER: PRJNA352727 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5001390_1.fastq.gz	Fastqsanger.gz
	SRR5001390_2.fastq.gz	Fastqsanger.gz
	SRR5001383_1.fastq.gz	Fastqsanger.gz
	SRR5001383_2.fastq.gz	Fastqsanger.gz
	SRR5001384_1.fastq.gz	Fastqsanger.gz

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RNA-seq transcriptome analysis in naïve and TNF-a-treated Sirt6-silenced YAMC cells to enrich for direct Sirt6 targets associated with inflammatory stimulation.

Project description:By comparing Sirt6-silenced YAMC cells to siControl-transfected YAMC cells, we found that there were 916 and 1,026 differentially expressed genes in the naïve and TNF-a treatment conditions respectively. We also found that there were 302 genes that were co-expressed differentially in both naïve and TNF-a treatment conditions between Sirt6-silenced and siControl-transfected YAMC cells.

2018-01-03 | GSE89620 | GEO

Dynamic Chromatin Localization of Sirt6 Shapes Stress- and Aging- Related Transcriptional Networks (Illumina)

Project description:Sirtuins (Sirt) are a family of enzymes that modify chromatin and other proteins to affect gene activity. Loss of Sirt6 leads to a progeria-like phenotype in mice, but the target of SIRT6 action has been elusive. Here we show that Sirt6 binds to thousands of gene promoters in a stress-inducible fashion, guided by the stress-responsive transcription factor NF-κB. Chromatin profiling by ChIP-chip analysis of Sirt6 and NF-KB component RelA combined with expression array data of wildtype, Sirt6 knockout and Sirt6 RelA double knockout cells demonstrates that RelA recruits Sirt6 to NF-KB targets in response to TNF-a induction and that many of these targets are important for senescence and aging. comparison of wild type, Sirt6-/- and Sirt6-/- RelA-/- MEF cells

2011-05-11 | E-GEOD-28585 | biostudies-arrayexpress

Dynamic Chromatin Localization of Sirt6 Shapes Stress- and Aging- Related Transcriptional Networks (ChIP-chip)

Project description:Sirtuins (Sirt) are a family of enzymes that modify chromatin and other proteins to affect gene activity. Loss of Sirt6 leads to a progeria-like phenotype in mice, but the target of SIRT6 action has been elusive. Here we show that Sirt6 binds to thousands of gene promoters in a stress-inducible fashion, guided by the stress-responsive transcription factor NF-?B. Chromatin profiling by ChIP-chip analysis of Sirt6 and NF-KB component RelA combined with expression array data of wildtype, Sirt6 knockout and Sirt6 RelA double knockout cells demonstrates that RelA recruits Sirt6 to NF-KB targets in response to TNF-a induction and that many of these targets are important for senescence and aging. comparison of wild type, RelA -/- and Sirt6-/- MEF cells

2011-05-11 | E-GEOD-28638 | biostudies-arrayexpress

Sirt6 study

Project description:This SuperSeries is composed of the following subset Series: GSE13206: Human shSIRT6 TNF-alpha timecourse GSE13207: Mouse Sirt6-/- TNF-alpha timecourse GSE13208: Mouse Sirt6-/- tissues GSE13209: Mouse Sirt6-/- RelA+/- tissues Refer to individual Series

2010-06-24 | E-GEOD-13272 | biostudies-arrayexpress

Dynamic Chromatin Localization of Sirt6 Shapes Stress- and Aging- Related Transcriptional Networks (ChIP-chip)

2011-05-11 | GSE28638 | GEO

Dynamic Chromatin Localization of Sirt6 Shapes Stress- and Aging- Related Transcriptional Networks (Illumina)

2011-05-11 | GSE28585 | GEO

CD4+ T cells treated with TNFalpha blocking agents during activation.

Project description:Objective. TNF? is a potent pro-inflammatory cytokine playing a pivotal role in several autoimmune diseases. Neutralizing TNF? inhibits T cell proliferation and IFN? production, and enhances suppressive capacity of regulatory T cells (Treg). Little is known about the mechanism of TNF? blocking agents on naïve T cell differentiation. Methods. Naïve CD4+ T cells were activated by dendritic cells (DC) in presence or absence of anti-TNF? agents. T cell polarization and activation was assessed during T cell differentiation. In addition, whole genome gene expression analysis was performed on anti-TNF?-treated T cells. Results. Neutralizing TNF? during priming of naïve CD4+ T cells by DC favors development of IL-10+ T helper (Th) cells at the expense of IFN? induction. TNF? inhibits IL-10 via TNFRII, which becomes expressed after naïve T cell activation. While initial CD4+ T cell activation was not affected, neutralization of TNF? negatively affected later stages of T cell priming by counteracting full T cell activation and survival. Whole genome gene expression analysis revealed a regulatory gene profile of anti-TNF?-treated T cells. Indeed, neutralizing TNF? during naïve T cell priming enhanced the suppressive function of anti-TNF?-treated T cells. Conclusion. Inhibition of TNF?–TNFRII interaction affects late stage effector T cell development and shifts the balance of Th cell differentiation towards IL-10 expressing regulatory T cells, which may be one of the beneficial mechanisms in TNF? blocking therapies. Naïve CD4+ T cells were CFSE labeled and co-cultured for 13 days with allogeneic dendritic cells in the presence or absence of anti-TNF? agents. After 13 days, the CFSElow T cells were FACS sorted. Samples were generated from three independent donors.

2014-06-25 | E-GEOD-42812 | biostudies-arrayexpress

Mus musculus

Project description:Mouse Sirt6-/- TNF-alpha timecourse

| PRJNA114029 | ENA

The effect of sirtuin 6 overexpression on TNFa stimulation.

Project description:SIRT6 has been implicated in a range of biological processes including inflammation, aging and the control of metabolism. Hence inhibitors or activators of SIRT6 have the potential to be therapeutics for a number of indications. Genome wide expression studies were used to investigate the effect of overexpression of SIRT6 and mutant SIRT6 on a wide range of NFκB dependent gene expression HEK293 cells were transfected with expression vectors encoding wild type SIRT6 or the H133W mutant followed by stimulation with TNFα for one hour.

2011-07-30 | E-GEOD-28548 | biostudies-arrayexpress

Sirt6 Deficiency Exacerbates Podocyte Injury and Proteinuria through Targeting Notch Signaling

Project description:Podocyte injury is a major determinant in proteinuric kidney disease and identification of potential therapeutic targets for preventing podocyte injury has clinical importance. Here, we show that histone deacetylase Sirt6 protects against podocyte injury through epigenetic regulation of Notch signaling. Sirt6 is downregulated in renal biopsies from patients with podocytopathies and its expression negatively correlates withglomerular filtration rate. Podocyte-specific deletion of Sirt6 exacerbates podocyte injury and proteinuria in two independent mouse models including diabetic nephropathy and adriamycin-induced nephropathy. Sirt6 has pleiotropic protective actions in podocytes including anti-inflammatory and anti-apoptotic effects, is involved in actin cytoskeleton maintenance, and promotes autophagy. Sirt6 also reduces urokinase plasminogen activator receptor expression, which is a key factor for podocyte foot process effacement and proteinuria. Mechanistically, Sirt6 inhibits Notch1 and Notch4 transcription by deacetylating the histone H3K9. We suggest Sirt6 as a potential therapeutic target in proteinuric kidney disease.

2017-06-20 | GSE100185 | GEO

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