This SuperSeries is composed of the SubSeries listed below.
Long noncoding RNAs regulate adipogenesis.
Specimen part, Disease
View SamplesAdipogenesis 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.
Long noncoding RNAs regulate adipogenesis.
Specimen part, Disease
View SamplesAdipogenesis 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.
Long noncoding RNAs regulate adipogenesis.
Specimen part, Cell line, Subject
View SamplesThe following abstract from the submitted manuscript describes the major findings of this work.
A role for peroxisome proliferator-activated receptor γ coactivator-1 in the control of mitochondrial dynamics during postnatal cardiac growth.
Specimen part
View SamplesSingle-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
Molecular architecture underlying fluid absorption by the developing inner ear.
Specimen part, Cell line, Subject
View SamplesBreast tumorigenesis involves modulation of gene expression.
Nucleotide excision repair deficiency is intrinsic in sporadic stage I breast cancer.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Linking DNA methyltransferases to epigenetic marks and nucleosome structure genome-wide in human tumor cells.
Specimen part, Cell line
View SamplesWe used microarrays to profile gene expression of NCCIT cells to study the link between epigenetic modifications and gene transcription.
Linking DNA methyltransferases to epigenetic marks and nucleosome structure genome-wide in human tumor cells.
Specimen part
View SamplesCompelling 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.
Energy metabolic reprogramming in the hypertrophied and early stage failing heart: a multisystems approach.
Sex, Age, Specimen part
View SamplesHigh-throughput gene expression profiling has become an important tool for investigating transcriptional activity in a variety of biological samples. To date, the vast majority of these experiments have focused on specific biological processes and perturbations. Here, we profiled gene expression from a diverse array of normal tissues, organs, and cell lines in mice. Keywords: multiple tissues
Expression analysis of G Protein-Coupled Receptors in mouse macrophages.
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