This SuperSeries is composed of the SubSeries listed below.
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.
Age, Specimen part, Disease
View SamplesLiver global gene expression patterns of 9 GNMT-knockout mice histopathologically determined to have non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) together with 10 MAT1A-knockout mice histopathologically determined to have steatosis and NASH. All these have their respective wild type patterns. These were analyzed to define signatures to study the pathogenesis of NAFLD-derived HCC, explore which subtypes of cancers can be investigated using mouse models and define a signature of HCC differential survival that can be used to characterize HCC subtypes of different survival derived from mixed etiologies.
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.
Age, Specimen part, Disease
View SamplesGlobal gene expression patterns of 2 human steatosis and 9 human non-alcoholic steatohepatitis (NASH) together with their respective control patterns were analyzed to define the non-alcoholic fatty liver disease (NAFLD) progression molecular characteristics and to define NASH early markers from steatosis.
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.
Specimen part, Disease
View SamplesLiver global gene expression patterns of 15-month-old MAT1A knockout mice histopathologically determined to have hepatocellular carcinoma (HCC). 5 samples are of tumoral tissue and 5 samples are of peritumoral tissue. All these have their respective wild type patterns. These were analyzed to define signatures to study the pathogenesis of NAFLD-derived HCC, explore which subtypes of cancers can be investigated using mouse models and define a signature of HCC differential survival that can be used to characterize HCC subtypes of different survival derived from mixed etiologies.
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.
Age, Specimen part, Disease
View SamplesThis experiment tests the hypothesis that interleukin-1 promotes SMC phenotypic modulation to a distinct inflammatory state relative to the growth factor PDGF-DD.
Interleukin-1β modulates smooth muscle cell phenotype to a distinct inflammatory state relative to PDGF-DD via NF-κB-dependent mechanisms.
No sample metadata fields
View SamplesWe investigated the global gene expression changes in normal and Brg1-deleted mesoderm differentiation of mouse embryonic stem cells. Overall design: RNAseq analysis of poly-adenylated RNA levels for 3 conditions: Day2 of differentiation, Day4 THF (Control), and Day4 4OHT (Brg1-deleted). 2 replicates per condition.
Brg1 modulates enhancer activation in mesoderm lineage commitment.
Cell line, Subject, Time
View SamplesInduced pluripotent stem cells (iPSCs) have been generated from various somatic cells under feeder-layer conditions. These feeder-derived iPSCs generated in different labs exhibit greater variability than between different traditional embryo derived hESC lines. For that reason, it is important to develop a standard and defined system for deriving autologous patient stem cells. We have generated iPSCs under feeder-free conditions using Matrigel coated vessels in chemically defined medium, mTeSR1. These feeder-free derived iPSCs are in many ways similar to feeder-derived iPSCs and also to hESCs, with respect to their pluripotent gene expression (OCT4, NANOG, SOX2), protein expression (OCT4, NANOG, SSEA4, TRA160) and differentiation capabilities.
Human induced pluripotent stem cells derived under feeder-free conditions display unique cell cycle and DNA replication gene profiles.
Specimen part
View SamplesIL-1 plays an important role in atherosclerosis, and alters expression of a number of genes involved in atherosclerotic plaque development and progression. Smooth muscle cells play important roles in atherosclerotic plaque formation and stability, so this study was undertaken to determine the global effects of IL-1b on gene expression in smooth muscle cells in vitro.
Genetic inactivation of IL-1 signaling enhances atherosclerotic plaque instability and reduces outward vessel remodeling in advanced atherosclerosis in mice.
Specimen part
View SamplesMyoblasts harvested from a postnatal day 2 WT and Foxj3 KO litter.
Foxj3 transcriptionally activates Mef2c and regulates adult skeletal muscle fiber type identity.
No sample metadata fields
View SamplesPurpose: To identify genes that are transcriptionally controlled by Notch signaling during zebrafish lateral line proneuromast formation. Methods: We isolated primordium cells from dissected tails of 36 hpf Tg((cldnB:GFP);Tg(cldnB:gal4) x Tg(UAS:nicd)) and sibling Tg((cldnB:GFP);Tg(cldnB:gal4)) embryos by FACS and performed RNASeq analysis. Results: Using an optimized data analysis workflow, we mapped about 26 million sequence reads per sample to the zebrafish genome (build danRer10) and identified 32,105 transcripts in the dissociated tails of WT and NICD zebrafish with TopHat workflow. Approximately 2% of the transcripts showed differential expression between the WT and NICD tails, with a fold change =0.5 and p value <0.01. Conclusion: RNASeq analyses revealed that Notch signaling cell-autonomously induces apical constriction and cell adhesion. Overall design: Zebrafish lateral line mRNA profiles of 36 hours wild type (WT) and NICD embryos were generated in triplicate, using HiSeq 2500 (Illumina).
Proliferation-independent regulation of organ size by Fgf/Notch signaling.
No sample metadata fields
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