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SRP098571
Homo sapiens
6 Downloadable Samples
Illumina HiSeq 2500
Description
Cellular replicative senescence, a state of permanent cell-cycle arrest that occurs following an extended period of cell division in culture, has been linked to organismal aging, tissue repair and tumorigenesis. In this study, we comparatively investigated the global lipid profiles and mRNA content of proliferating and senescent-state BJ fibroblast cells. We found that both the expression levels of lipid-regulating genes, as well as the abundance of specific lipid families, are actively regulated. We further found that 19 polyunsaturated triacylglycerol species showed the most prominent changes during replicative senescence. We argue that diversion of polyunsaturated fatty acids to glycerolipid biosynthesis could be responsible for the accumulation of specific triacylglycerols. This, in turn, could be one of the cellular mechanisms to prevent lipotoxicity under increased oxidative stress conditions observed during replicative senescence. Collectively, our results place regulation of specific lipid species to a central role during replicative senescence. Overall design: We sequence total RNA from 3 early PD and 3 senesent human BJ cell lines to detect the expressional differences between early PD and senescent cells.
Publication Title
Regulation of lipids is central to replicative senescence.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This dataset contains Affymetrix Mouse Genome 430 2.0 Array data obtained from K7M2 cells over-expressing ezrinT567A and the wild-type
Publication Title
Dysregulation of ezrin phosphorylation prevents metastasis and alters cellular metabolism in osteosarcoma.
Sample Metadata Fields
Cell line
View Samples- Mus musculus, Homo sapiens
- 30 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Characterisation of cisplatin-induced transcriptomics responses in primary mouse hepatocytes, HepG2 cells and mouse embryonic stem cells shows conservation of regulating transcription factor networks.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The transcriptomic changes induced in the human liver cell line HepG2 by 7M of cisplatin after treatment for 12, 24 and 48h
Publication Title
Characterisation of cisplatin-induced transcriptomics responses in primary mouse hepatocytes, HepG2 cells and mouse embryonic stem cells shows conservation of regulating transcription factor networks.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The transcriptomic changes induced in primary mouse hepatocytes (C57BL/6 ) by 7M of cisplatin after treatment for 24 and 48h
Publication Title
Characterisation of cisplatin-induced transcriptomics responses in primary mouse hepatocytes, HepG2 cells and mouse embryonic stem cells shows conservation of regulating transcription factor networks.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 179 Downloadable Samples
- Illumina HiSeq 2000
Description
Progressive failure of insulin-producing beta cells is the central event leading to diabetes, yet the signalling networks controlling beta cell fate remain poorly understood. Here we show that SRp55, a splicing factor regulated by the diabetes susceptibility gene GLIS3, has a major role in maintaining function and survival of human beta cells. RNA-seq analysis revealed that SRp55 regulates the splicing of genes involved in cell survival and death, insulin secretion and JNK signalling. Specifically, SRp55-mediated splicing changes modulate the function of the pro-apoptotic proteins BIM and BAX, JNK signalling and endoplasmic reticulum stress, explaining why SRp55 depletion triggers beta cell apoptosis. Furthermore, SRp55 depletion inhibits beta cell mitochondrial function, explaining the observed decrease in insulin release. These data unveil a novel layer of regulation of human beta cell function and survival, namely alternative splicing modulated by key splicing regulators such as SRp55 that may crosstalk with candidate genes for diabetes. Overall design: Five independent preparations of EndoC-ßH1 cells exposed to control (siCTL) or SRp55 (siSR#2) siRNAs
Publication Title
SRp55 Regulates a Splicing Network That Controls Human Pancreatic β-Cell Function and Survival.
Sample Metadata Fields
Treatment, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina Genome Analyzer, Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
RNA-Seq provides new insights in the transcriptome responses induced by the carcinogen benzo[a]pyrene.
Sample Metadata Fields
Cell line, Compound, Time
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Whole-genome transcriptome measurements are pivotal for characterizing carcinogenic mechanisms of chemicals and predicting toxic classes, such as genotoxicity, from in vitro and in vivo assays. DNA microarrays have evolved as the gold standard for this purpose. In recent years deep sequencing technologies have been developed that hold the promise of measuring the transcriptome with RNA-seq in a more accurate and unbiased manner than microarrays. So far, however, few applications have been published that assess the performance of RNA-seq within a toxicogenomics context. Here, we applied RNA-seq for the characterization of the in vitro transcriptomic responses in HepG2 cells upon exposure to benzo[a]pyrene (BaP), a well-known DNA damaging carcinogen. We demonstrate the performance of RNA-seq with respect to the identification of differentially expressed genes and associated pathways, in comparison with microarray technology. RNA-seq data generates more complete and thus accurate data on differentially expressed genes and affected pathways than microarrays. Additionally, we highlight the potential of RNA-seq for characterizing mechanisms related to alternative splicing and thereby gathering new information. Exposure to BaP alters the isoform distribution for many genes, including regulators of cell death and DNA repair such as TP53, BCL2 and XPA, which are relevant for genotoxic responses. Finally, we demonstrate that RNA-seq enables to investigate allele-specific gene expression, although no changes for that could be observed. Our results provide evidence that RNA-seq is a powerful tool for toxicology which, compared to microarrays, is capable of adding valuable information at the transcriptome level for characterizing toxic effects caused by chemicals.
Publication Title
RNA-Seq provides new insights in the transcriptome responses induced by the carcinogen benzo[a]pyrene.
Sample Metadata Fields
Cell line, Compound, Time
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
TIMP-4 overexpression increases tumor burden in mice, promotes progenitor cell phenotype and sensitizes cells to apoptosis, by relying on NFkB signaling
Publication Title
Tissue inhibitor of metalloproteinases-4 (TIMP-4) regulates stemness in cervical cancer cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus, Homo sapiens
- 25 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Neurons and endothelial cells were identified by immunohistochemistry in human brains, isolated by laser-capture-microdissection and used to find genes preferentially expressed in the two cell types.
Publication Title
Evolution of neuronal and endothelial transcriptomes in primates.
Sample Metadata Fields
Sex, Specimen part
View Samples