Snt2 is a yeast chromatin-interacting protein whose function has not been well characterized, that was recently shown to associate with Ecm5 and the Rpd3 deacetylase. Using chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq), we show that in response to H2O2, Snt2 and Ecm5 colocalize to promoters of genes involved in various aspects of the environmental stress response. By integrating these ChIP-seq results with expression analysis, we identify a key set of target genes that require Snt2 for proper expression after H2O2 stress. Finally, by mapping Snt2 and Ecm5 localization before and after rapamycin treatment, we identify a subset of H2O2-specific Snt2 and Ecm5 target promoters that are also targeted in response to rapamycin. Our results establish a function for Snt2 in regulating transcriptional changes in response to oxidative stress, and suggest Snt2 may have a role in additional stress pathways. Overall design: RNA-seq analysis to look at gene expression levels in wild-type, snt2 deletion, or ecm5 deletion strains before or 0.5 hours after treatment with H2O2 (final concentration 0.4 mM). This sequencing was done on biological triplicate samples.
The yeast Snt2 protein coordinates the transcriptional response to hydrogen peroxide-mediated oxidative stress.
Subject
View SamplesPurpose: The goal of this study is to analyze the transcriptional pathways regulated by Fbxo22 and Keap1 in mouse lung adeno carcinoma cells. Methods: mouse lung adeno carcinoma cells either Keap1 wild type (KP) or mutant (KPK), have been transfected for 3 days with siRNA targeting Fbxo22. Knock down efficiency has been evaluated by western blot (using specific antibody for Fbxo22) and qPCR (using specific oligos for Fbxo22) . Results: The transcriptomic analysis helps us to support our finding that loss of either Keap1 or Fbxo22 induces metastases Overall design: All 12 samples generated by deep sequencing in triplicate
Nrf2 Activation Promotes Lung Cancer Metastasis by Inhibiting the Degradation of Bach1.
Specimen part, Subject
View SamplesThe phenotypically characterized hTERT immortalized porcine olfactory bulb neuroblast cell line (OBGF400) was subjected to an extensive whole genome-scaled expression profile for establishing their use as an in vitro neuronal disease model system.
Transcriptome profile and cytogenetic analysis of immortalized neuronally restricted progenitor cells derived from the porcine olfactory bulb.
Cell line
View SamplesInfection with acute and chronic strains of LCMV (Armstrong (ARM) and Clone 13 (C13), respectively) leads to massive proliferation of monocytic cells contemporaneously with peak of the anti-viral CD8+ T cell response. These cells return to nave levels following ARM infection. However, during C13 infection these cells are sustained at high levels and gain a T cell suppressive function at day 14 post infection. The mechanisms by which these cells are induced to proliferate and impair T cell function during chronic LCMV infection are largely unknown. To address this, we analyzed gene expression profiles using microarray analysis of purified splenic monocytic cells (CD11b+ Ly6Chi Gr-1low) from nave mice, or day 14 LCMV ARM or LCMV C13 infected mice.
Chronic but not acute virus infection induces sustained expansion of myeloid suppressor cell numbers that inhibit viral-specific T cell immunity.
Specimen part
View SamplesComparison of transcriptional profiles of human umbilical vein endothelial cells (HUVECs) expressing wild-type vs. VM-causative mutant forms of TIE2/TEK.
Venous malformation-causative TIE2 mutations mediate an AKT-dependent decrease in PDGFB.
Specimen part
View SamplesThe aim of the current study was to identify molecular markers for articular cartilage that can be used for the quality control of tissue engineered cartilage. Therefore a genom-wide expression analysis was performed using RNA isolated from articular and growth plate cartilage, both extracted from the knee joints of minipigs.
Identification of molecular markers for articular cartilage.
Specimen part
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