In this study we performed a genome wide analysis of the entire complement of mRNAs in clear cell renal cell carcinomas (ccRCC) by means of the Affymetrix Exon Array platform. The analyses were performed both at gene and exon level.
Genome-wide analysis of differentially expressed genes and splicing isoforms in clear cell renal cell carcinoma.
Sex, Age, Specimen part, Subject
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Dynamic Transcriptional and Epigenetic Regulation of Human Epidermal Keratinocyte Differentiation.
Specimen part, Disease
View SamplesGene expression profiling of progenitor and differentiated keratinocytes by Affymetrix microarray
Dynamic Transcriptional and Epigenetic Regulation of Human Epidermal Keratinocyte Differentiation.
Specimen part
View SamplesThe capacity of the hematopoietic system to promptly respond to peripheral demands relies on adequate pools of progenitors able to transiently proliferate and differentiate in a regulated manner. However, little is known about factors that may restrain progenitor maturation to maintain their reservoirs. In addition to a profound defect in hematopoietic stem cell (HSC) self-renewal, conditional knockout mice for the Pbx1 proto-oncogene have a significant reduction in lineage-restricted progenitors, including common myeloid progenitors (CMPs) and, to a lesser extent, granulocyte-monocyte progenitors (GMPs).
Pbx1 restrains myeloid maturation while preserving lymphoid potential in hematopoietic progenitors.
Age, Specimen part
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Pbx1 regulates self-renewal of long-term hematopoietic stem cells by maintaining their quiescence.
Age, Specimen part
View SamplesSelf-renewal is a defining characteristic of stem cells, however the molecular pathways underlying its regulation are poorly understood. Here we demonstrate that conditional inactivation of the Pbx1 proto-oncogene in the hematopoietic compartment results in a progressive loss of long-term hematopoietic stem cells (LT-HSCs) that is associated with concomitant reduction in their quiescence, leading to a defect in the maintenance of self-renewal as assessed by serial transplantation. Transcriptional profiling revealed that multiple stem cell maintenance factors are perturbed in Pbx1-deficient LT-HSCs, which prematurely express a large subset of genes, including cell cycle regulators, normally expressed in non-self-renewing multipotent progenitors. A significant proportion of Pbx1-dependent genes are associated with the Tgf-b pathway, which serves a major role in maintaining HSC quiescence. Pbx1-deficient LT-HSCs are unable to up-regulate the cyclin dependent kinase inhibitor p57 in response to Tgf-b, providing a mechanism through which Pbx1 maintenance of stem cell self-renewal is achieved.
Pbx1 regulates self-renewal of long-term hematopoietic stem cells by maintaining their quiescence.
Age, Specimen part
View SamplesSelf-renewal is a defining characteristic of stem cells, however the molecular pathways underlying its regulation are poorly understood. Here we demonstrate that conditional inactivation of the Pbx1 proto-oncogene in the hematopoietic compartment results in a progressive loss of long-term hematopoietic stem cells (LT-HSCs) that is associated with concomitant reduction in their quiescence, leading to a defect in the maintenance of self-renewal as assessed by serial transplantation. Transcriptional profiling revealed that multiple stem cell maintenance factors are perturbed in Pbx1-deficient LT-HSCs, which prematurely express a large subset of genes, including cell cycle regulators, normally expressed in non-self-renewing multipotent progenitors.
Pbx1 regulates self-renewal of long-term hematopoietic stem cells by maintaining their quiescence.
Age, Specimen part
View SamplesMany studies have characterized the results of shear stress changes on cultured endothelial cells in different bioreactor systems. However it is still unclear how an invasive intervention like stent procedure may influence the transcriptional response of endothelium.
Vascular injury post stent implantation: different gene expression modulation in human umbilical vein endothelial cells (HUVECs) model.
Specimen part
View SamplesMyc is a multifaceted bHLHZip transcription factor deregulated in the majority of human cancers. How to target Myc for cancer therapy is unclear, given its involvement in a variety of key functions in healthy cells. We used microarrays to capture the cellular transcriptional response to Omomyc a Myc interfering molecule acting at the level of protein protein interactions that demonstrated a remarkable therapeutic efficacy in transgenic mouse cancer models.
No associated publication
Specimen part, Cell line, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part
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