Many 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 SamplesIn 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
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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 SamplesThis SuperSeries is composed of the SubSeries listed below.
let-7 Modulates Chromatin Configuration and Target Gene Repression through Regulation of the ARID3B Complex.
Specimen part, Cell line
View SamplesExpression of let-7i results in transcriptome alteractions in head and neck cancer cell line, OECM1.
let-7 Modulates Chromatin Configuration and Target Gene Repression through Regulation of the ARID3B Complex.
Cell line
View SamplesRecently a new neonatal diabetes syndrome, Mitchell-Riley syndrome, was discovered. To identify the genetic cause of the syndrome homozygosity mapping was used, several chromosomal regions were linked to Mitchell-Riley syndrome. In situ hybridization of genes from one such region using model organism Xenopus laevis identified RFX6 as a potential candidate gene; mutant forms of RFX6 were subsequently found in Mitchell-Riley patients. Analysis of the expression pattern of RFX6 in Xenopus development shows it is expressed broadly in the endoderm early in development, and later RFX6 becomes restricted to the endocrine cells of the gut and pancreas. Morpholino knockdown of RFX6 in Xenopus caused a loss of pancreas marker gene expression. Injection of exogenous wild type RFX6 rescued the morpholino phenotype in Xenopus tadpoles. Attempts to rescue the loss-of-function phenotype using mutant forms of RFX6 found in Mitchell-Riley patients were unsuccessful suggesting the changes lead to loss-of-function and could be the cause of Mitchell-Riley syndrome. Microarray analysis of gene expression in knockdown tissue suggested a downregulation in marker genes for lung, stomach and heart, ambiguous results for the liver, and an upregulation in kidney marker gene expression. RT-PCR and in situ hybridization confirms a loss of lung, stomach and heart gene expression, no change in liver marker hex and an upregulation in kidney marker KcnJ1. The fact that the morpholino phenotype affects multiple organs suggests that RFX6 has a broad role early in endoderm development.
Functional analysis of Rfx6 and mutant variants associated with neonatal diabetes.
Specimen part, Treatment
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
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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
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