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GSE83370
Homo sapiens
12 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Sample Metadata Fields
Specimen part, Disease stage, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Matrix induced effects on gene expression in HeLa and MDA-MB-231 cells
Publication Title
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
Illumina HiSeq 2500
Description
gene expression data from 3 pairs of cancer associated fibroblasts and normal fibroblasts from the same individual Overall design: mRNA seq data from 3 normal and 3 cancer associated fibroblast cell lines
Publication Title
Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription.
Sample Metadata Fields
Specimen part, Disease stage, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The following abstract from the submitted manuscript describes the major findings of this work.
Publication Title
A role for peroxisome proliferator-activated receptor γ coactivator-1 in the control of mitochondrial dynamics during postnatal cardiac growth.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 199 Downloadable Samples
- Illumina HiSeq 1000
Description
Single-cell RNA-seq analysis of pre- and postnatal mouse endolymphatic sac demonstrates two types of differentiated cells distinguished by their mRNA expression signatures. Overall design: mRNA-seq profiles from 213 single cells from embryonic day 12.5, 16.5, postnatal day 5 and 30 mouse endolymphatic sac were analyzed
Publication Title
Molecular architecture underlying fluid absorption by the developing inner ear.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Breast tumorigenesis involves modulation of gene expression.
Publication Title
Nucleotide excision repair deficiency is intrinsic in sporadic stage I breast cancer.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 27 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Long noncoding RNAs regulate adipogenesis.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 11 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Adipogenesis involves the regulation of hundreds of genes by several well-studied proteins, but the role of long, noncoding RNAs in this process has not been defined. We track the regulation of hundreds of lncRNAs during adipocyte differentiation, and find several that are essential for this process.
Publication Title
Long noncoding RNAs regulate adipogenesis.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina Genome Analyzer
Description
Adipogenesis involves the regulation of hundreds of genes by several well-studied proteins, but the role of long, noncoding RNAs in this process has not been defined. We track the regulation of hundreds of lncRNAs during adipocyte differentiation, and find several that are essential for this process. Overall design: We extractedbrown and white primary adipocytes and pre-adipocytes and profiled lncRNA expresssion via mRNA-Seq. We also profiled cultured, differentiated adipocytes to verify that we could recapitulate the adipocyte expression profile in preparation for a loss-of-function screen for essential adipogenic lincRNAs.
Publication Title
Long noncoding RNAs regulate adipogenesis.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 30 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Compelling evidence suggests that mitochondrial dysfunction contributes to the pathogenesis of heart failure, including defects in the substrate oxidation, and the electron transport chain (ETC) and oxidative phosphorylation (OXPHOS). However, whether such changes occur early in the development of heart failure, and are potentially involved in the pathologic events that lead to cardiac dysfunction is unknown. To address this question, we conducted transcriptomic/metabolomics profiling in hearts of mice with two progressive stages of pressure overload-induced cardiac hypetrophy: i) cardiac hypertrophy with preserved ventricular function achieved via transverse aortic constriction for 4 weeks (TAC) and ii) decompensated cardiac hypertrophy or heart failure (HF) caused by combining 4 wk TAC with a small apical myocardial infarction. Transcriptomic analyses revealed, as shown previously, downregulated expression of genes involved in mitochondrial fatty acid oxidation in both TAC and HF hearts compared to sham-operated control hearts. Surprisingly, however, there were very few changes in expression of genes involved in other mitochondrial energy transduction pathways, ETC, or OXPHOS. Metabolomic analyses demonstrated significant alterations in pathway metabolite levels in HF (but not in TAC), including elevations in acylcarnitines, a subset of amino acids, and the lactate/pyruvate ratio. In contrast, the majority of organic acids were lower than controls. This metabolite profile suggests bottlenecks in the carbon substrate input to the TCA cycle. This transcriptomic/metabolomic profile was markedly different from that of mice PGC-1a/b deficiency in which a global downregulation of genes involved in mitochondrial ETC and OXPHOS was noted. In addition, the transcriptomic/metabolomic signatures of HF differed markedly from that of the exercise-trained mouse heart. We conclude that in contrast to current dogma, alterations in mitochondrial metabolism that occur early in the development of heart failure reflect largely post-transcriptional mechanisms resulting in impedance to substrate flux into the TCA cycle, reflected by alterations in the metabolome.
Publication Title
Energy metabolic reprogramming in the hypertrophied and early stage failing heart: a multisystems approach.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples