The present study was to investigate the differentially expressed genes in 24-hour-old (containing proliferative cardiomyocytes), 7-day-old (containing the burst of proliferative cardiomyocytes), and 10-week-old (containing growth-arrested cardiomyocytes) C57BL/6 mouse hearts using global gene expression profiles.
Global gene expression analysis combined with a genomics approach for the identification of signal transduction networks involved in postnatal mouse myocardial proliferation and development.
Specimen part
View SamplesExpression data from human induced pluripotent stem cells(iPSCs) and Human foreskin fibroblasts (HFFs) with treatment actinomycin D
Global analysis reveals multiple pathways for unique regulation of mRNA decay in induced pluripotent stem cells.
Specimen part, Treatment, Time
View SamplesAlmost all cellular mRNAs terminate in a 3 poly(A) tail, the removal of which can induce both translational silencing and mRNA decay. Mammalian cells encode many poly(A)-specific exoribonucleases but their individual roles are poorly understood. Here, we undertook an analysis of the role of PARN deadenylase in mouse myoblasts using global measurements of mRNA decay rates. Our results reveal that a discrete set of mRNAs exhibit altered mRNA decay as a result of PARN depletion and that stabilization is associated with increased poly(A) tail length and translation. We determined that stabilization of mRNAs does not generally result in their increased abundance supporting the idea that mRNA decay is coupled to transcription. Importantly, PARN knockdown has wide ranging effects on gene expression that specifically impact the extracellular matrix and cell migration. Finally, although PARN has its own unique target transcripts it also influences some genes whose expression is modulated by other deadenylases.
The PARN deadenylase targets a discrete set of mRNAs for decay and regulates cell motility in mouse myoblasts.
Specimen part, Cell line
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Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells.
Specimen part, Cell line
View SamplesDramatic changes in gene expression occur in response to extracellular stimuli and during differentiation. Although transcriptional effects are important, alterations in mRNA decay also play a major role in achieving rapid and massive changes in mRNA abundance. Moreover, just as transcription factor activity varies between different cell types, the factors influencing mRNA decay are also cell-type specific. We have established the rates of decay for over 7000 transcripts expressed in mouse C2C12 myoblasts.
Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells.
Specimen part, Cell line
View SamplesWe harvested the heart from transgenic mice with cardiac specific overexpression of Sirt1 (Tg-Sirt1) and non-transgenic (NTg) control littermate at 3 months of age and then microarray analyses were conducted.
Sirt1 regulates aging and resistance to oxidative stress in the heart.
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View SamplesDramatic changes in gene expression occur in response to extracellular stimuli and during differentiation. Although transcriptional effects are important, alterations in mRNA decay also play a major role in achieving rapid and massive changes in mRNA abundance. Moreover, just as transcription factor activity varies between different cell types, the factors influencing mRNA decay are also cell-type specific.GREs are recognized by CUGBP1, an RNA-binding protein and instability factor whose function is affected in several neuromuscular diseases. To dectect the mRNA associated with CUGBP1, we utilized RNA immunoprecipitation followed by microarray (RIP-Chip) to identify CUGBP1-associated transcripts.
Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells.
Specimen part
View SamplesDespite education and aggressive treatment, breast cancer (BC) remains a clinical problem. BC cells (BCCs) can migrate early to metastatic sites where they may exist in cellular dormancy for decades. Presently, there are no consensus markers for cancer stem cells (CSCs) that are involved in tumor initiation and progression, and drug resistance. The current designation of CSCs might comprise similar tumor initiating cells, but at different developmental phase. In order to understand these differences, we developed a working hierarchy of BCCs. We initiated the studies in which three BCC subsets were selected based on the relative expressions of the stem cell-linked genes, Octamer4A (Oct4A). The sorted BCCs were subjected to array analyses using Affymetrix gene chip. Hierarchical clustering indicated distinct gene expression among the three subsets. Differential gene expressions of membrane proteins validated three novel genes, TMEM-98, GPR64 and FAT4. These three genes, in combination of known markers for CSCs, CD44, CD24, aldehyde dehydrogenase 1 (ALDH1) and Oct4A, were used to stratify BCCs led to a working hierarchy of BCCs. The validity of the hierarchical BCCs was applied to blood samples from patients, during relapse, and before and after treatment. These studies resulted in the patients grouped with distinct BCCs in the circulation. The relevance of the latter findings are discussed with regards to prediction of treatment response and time of BC relapse. The findings require a larger cohort of patients in a prospective multi-center study. The stratification could be important to understand treatment response, strategies for alternative approaches, and an understanding of the interaction between particular BCC subsets and the tissue microenvironment.
Evaluation of a developmental hierarchy for breast cancer cells to assess risk-based patient selection for targeted treatment.
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
ATRX, DAXX or MEN1 mutant pancreatic neuroendocrine tumors are a distinct alpha-cell signature subgroup.
Specimen part
View SamplesGene expression profiling of PanNETs patients samples were performed to understand genotype to phenotype correlations, novel molecular subtypes and cell of origin
ATRX, DAXX or MEN1 mutant pancreatic neuroendocrine tumors are a distinct alpha-cell signature subgroup.
Specimen part
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