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RNA Sequencing facilitates quantitative analysis of differently expressed genes with GA or SKN treatment in rheumatoid fibroblast-like synoviocytes

ABSTRACT: To explore downstream gene expression profile of PKM2,we evaluated the transcriptome of GA- or SKN-treated RA FLSs compared to untreated control using RNA sequencing analysis. The data were analyzed for differential expression with a nominal P<0.05. GA Treatment induced downregulation of 46 genes and upregulation of 58 genes compared to DMSO treatment. SKN treatment resulted in downregulation of 14 genes and upregulation of 27 genes compared to DMSO treatment.A Venn diagram showed the overlap of the significantly expressed genes between GA and SKN treatment. We found that in the overlap of both GA and SKN treatment, STAT5A and ARHGAP11A were significantly downregulated, and THAP6 and AHRR were significantly upregulated.

ORGANISM(S): Homo sapiens

PROVIDER: GSE155766 | GEO | 2020/08/06

REPOSITORIES: GEO

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SKN-1-dependent oxidative stress response in C. elegans

Project description:Oxidative stress may play a role in normal aging. SKN-1 is a transcription factor necessary for intestine development in Caenorhabditis elegans, which also regulates the response to oxidative stress post-embryonically. Using DNA microarrays, we found that oxidative stress induces the antioxidant response, the heat shock response, and detoxification genes, while the expression of genes involved in homeostasis, development, and reproduction were decreased. Both up-regulated and down-regulated genes can be wholly, partially, or not at all dependent on SKN-1 action. However, induction of the heat shock response by oxidative stress was not affected by SKN-1 removal. Keywords: stress response

2007-11-01 | GSE9301 | GEO

TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-Autonomously in Caenorhabditis elegans

Project description:The Caenorhabditis elegans oxidative stress response transcription factor, SKN-1, is essential for the maintenance of redox homeostasis and is a functional ortholog of the Nrf family of transcription factors. The numerous levels of regulation that govern these transcription factors underscore their importance. Here, we add a thioredoxin, encoded by trx-1, to the expansive list of SKN-1 regulators. We report that loss of trx-1 promotes nuclear localization of intestinal SKN-1 in a redox-independent, cell non-autonomous fashion from the ASJ neurons. Furthermore, this regulation is not general to the thioredoxin family, as two other C. elegans thioredoxins TRX-2 and TRX-3 do not play a role in this process. Moreover, TRX-1-dependent regulation requires signaling from the p38 MAPK signaling pathway. However, while TRX-1 regulates SKN-1 nuclear localization, SKN-1 transcriptional activity remains largely unaffected. Interestingly, RNA-Seq revealed that loss of trx-1 elicits a general, organism-wide down-regulation of several classes of genes; those encoding for collagens and lipid transport and localization being most prevalent. However, one prominent lipase-related gene, lips-6, is highly up regulated upon loss of trx-1 in a skn-1-dependent manner. Together, these results uncover a novel role for a thioredoxin in regulating intestinal SKN-1 nuclear localization in a cell non-autonomous manner, thereby contributing to the understanding of the processes involved in maintaining redox homeostasis throughout an organism. Four samples were analyzed: Two nematode strains were analyzed, each under non-stressed and stressed (10mM NaAs) conditions

2016-04-01 | E-GEOD-77976 | biostudies-arrayexpress

Skn-1-deficient effect on the gastrocnemius

Project description:Analysis of gastrocnemius from male wild type(WT) and Skn-1-deficient mice. Skn-1-deficient mice have reduced body weight with low body fat due to increased energy expenditure. Results provide insight into the molecular mechanisms up-regulating metabolism.

2017-02-11 | GSE76936 | GEO

RNA Sequencing facilitates quantitative analysis of differently expressed genes with GA or SKN treatment in rheumatoid fibroblast-like synoviocytes

Project description:RNA Sequencing facilitates quantitative analysis of differently expressed genes with GA or SKN treatment in rheumatoid fibroblast-like synoviocytes

| PRJNA655506 | ENA

RNA-seq of C. Elegans control vs SKN-1b mutant

Project description:The difference in translation between CGCM and SKN-1b mutant

2020-08-13 | E-MTAB-8253 | biostudies-arrayexpress

Identification of Transcription Factor SKN-1::GFP Binding Regions in L1

Project description:modENCODE_submission_2622 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: OP178(made_by : S Kim tags : GFP::3xFlag mutagen : Bombard outcross : 3 genotype : unc119(ed3);wgIs178(skn-1::TY1 EGFP FLAG;unc119) official name : WBGene00004804 ); Developmental Stage: fed L1; Genotype: unc119(ed3);wgIs178(skn-1::TY1 EGFP FLAG;unc119); Sex: Hermaphrodite; EXPERIMENTAL FACTORS: Developmental Stage fed L1; Target gene skn-1; Strain OP178(made_by : S Kim tags : GFP::3xFlag mutagen : Bombard outcross : 3 genotype : unc119(ed3);wgIs178(skn-1::TY1 EGFP FLAG;unc119) official name : WBGene00004804 ); temp (temperature) 20 degree celsius Series_type: CHIP-seq

2011-02-18 | E-GEOD-25810 | biostudies-arrayexpress

RNA-seq analysis of germline stem cell removal and loss of SKN-1 in C. elegans

Project description:In C. elegans, ablation of germline stem cells (GSCs) extends lifespan, but also increases fat accumulation and alters lipid metabolism, raising the intriguing question of how these effects might be related. Here we show that a lack of GSCs results in a broad transcriptional reprogramming, in which the conserved detoxification regulator SKN-1/Nrf increases stress resistance, proteasome activity, and longevity. SKN-1 also activates diverse lipid metabolism genes and reduces fat storage, thereby alleviating the increased fat accumulation caused by GSC absence. Surprisingly, SKN-1 is activated by signals from this fat, which appears to derive from unconsumed yolk that was produced for reproduction. We conclude that SKN-1 plays a direct role in maintaining lipid homeostasis, in which it is activated by lipids. This SKN-1 function may explain the importance of mammalian Nrf proteins in fatty liver disease, and suggests that particular endogenous or dietary lipids might promote health through SKN-1/Nrf.

2015-07-21 | GSE63075 | GEO

TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-Autonomously in Caenorhabditis elegans

2016-04-01 | GSE77976 | GEO

Transcriptional redirection of activated SKN-1/NRF2 abates the negative metabolic outcomes of a perceived pathogen infection

Project description:Optimal health requires perpetual transcriptional fidelity of gene expression. SKN-1/NRF2 is a cytoprotective transcription factor in C. elegans that regulates the expression of cellular defenses during stress, including: nutrient deprivation, redox imbalance, and xenobiotic and pathogen exposure. Constitutive activation of SKN-1 results in pleiotropic outcomes, including shortened lifespan and protective redistribution of somatic fat to the germline. We measured lipid distribution between the soma and germ tissues after manipulation of SKN-1 activity. Modulating the epigenetic landscape refines SKN-1 activity away from innate immunity targets and alleviates negative metabolic outcomes. Similarly, paraquat exposure redirects SKN-1 activity toward oxidative stress responses and away from pathogen response genes, which restores lipid distribution across tissues. Lastly, activating p38 MAPK signaling is sufficient to drive SKN-1-dependent loss of somatic fat. These data reveal a coordination of organismal metabolic homeostasis with pathogen responses and identifies mechanisms for counteracting the pleiotropic consequences of aberrant transcriptional activity.

2019-10-15 | GSE123531 | GEO

Role of SKN-1 in dpy-7 and osmotic gene induction

Project description:We report the use of mRNA sequencing to analyze the role of SKN-1 in regulation of genes under two conditions, dpy-7 mutants and high osmolarity.

2018-02-12 | GSE107704 | GEO

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