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Mus musculus
10 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Multiple Endocrine Neoplasia Tumor Syndrome type 1 (MEN 1) is an autosomal dominant tumor syndrome affecting individuals with a heterozygous germline mutaion of the MEN1 gene. MEN 1 carriers commonly develop parathyroid, anterior pituitary, duodenal and pancreatic endocrine tumors. The phenotype of existing mouse models for the MEN 1 syndrome, with a germline heterozygous (hz) Men1 gene inactivation, show close resemblance to the human MEN 1 syndrome. Menin, the protein encoded for by the MEN1/Men1 gene, lacks homology with known proteins, and evidence of its involvement in different cellular processes is steadily growing. Several interaction partners have been identified, involving different interaction sites on the menin protein. Accumulating evidence suggests a role for menin in transcriptional regulation, cell cycle control, apoptosis, chromatin modification and DNA damage response and repair. Loss of heterozygosity (LOH) of the MEN1 gene precedes tumor formation in the MEN 1 heterozygous pancreas. We set out to determine if there is a change in gene expression early on in the hz islet, as compared with islets in wildtype (wt) littermates, long before the LOH events occur. We performed a global mRNA expression microarray on islets from young, five-week-old, hz Men1 mice and their wt littermates, and we have subsequently corroborated a subset of the findings on the qPCR and protein level.
Publication Title
Accelerated proliferation and differential global gene expression in pancreatic islets of five-week-old heterozygous Men1 mice: Men1 is a haploinsufficient suppressor.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus, Homo sapiens
- 23 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.
Publication Title
VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.
Publication Title
VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 32 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Gene expression profiles from the aortic arch of Ldlr-/-Apob100/100 Mttpflox/flox Mx1-Cre mice at different stages of atherosclerosis development
Publication Title
Transcriptional profiling uncovers a network of cholesterol-responsive atherosclerosis target genes.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
Illumina HiSeq 2000
Description
RNA sequencing data for four cell lines representing different stages during malignant transformation.
Publication Title
Majority of differentially expressed genes are down-regulated during malignant transformation in a four-stage model.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 275 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Tissue samples have been isolated during corornary artery by-pass grafting (CABG)surgery from the atheroscelrotic arterial wall (AAW, aortic root puncture for proxmal ligation of by-pass vessel), non-atherosclertoci arterial wall (NAAW, distal part of mammary artery used a graft for LAD), liver, skeletal muscle (Recturs m), pericardial mediastinal visceral fat) in CAD patients. Carotid lesions samples from 25 validation patients.
Publication Title
Multi-organ expression profiling uncovers a gene module in coronary artery disease involving transendothelial migration of leukocytes and LIM domain binding 2: the Stockholm Atherosclerosis Gene Expression (STAGE) study.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 31 Downloadable Samples
- Affymetrix Human Gene 2.1 ST Array (hugene21st)
Description
Atopic dermatitis (AD) is a common inflammatory skin disease with underlying defects in epidermal function and immune responses. The goal of this study was to investigate differences in gene expression in lesional skin from patients with mild extrinsic or intrinsic AD compared to skin from healthy controls and from lesional psoriasis skin. The aim was to identify differentially expressed genes involved in skin barrier formation and inflammation, and to compare our results with those reported for patients with moderate and severe AD.
Publication Title
Distinct molecular signatures of mild extrinsic and intrinsic atopic dermatitis.
Sample Metadata Fields
Specimen part, Disease
View Samples
GSE104092- Sus scrofa
- 19 Downloadable Samples
- Porcine Gene 1.1 ST Array (porgene11st)
Description
We aimed to determine the infect of Ascaris suum infection on mucosal immune pathways in pigs
Publication Title
Ascaris Suum Infection Downregulates Inflammatory Pathways in the Pig Intestine In Vivo and in Human Dendritic Cells In Vitro.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The present study reports an unbiased analysis of the genetic profile and regulation of NKG2D expressing CD4 T-cells.An Affymetrix microarray analysis was used to explore the genetic profile of NKG2D+ versus NKG2D- CD4 T-cells. The genetic profile was studied by single gene analysis and gene set enrichment analysis. I found that several immune regulatory receptors was regulated differently in NKG2D+ versus NKG2D- CD4 T-cells. Futhermore, I found that NKG2D+ CD4 T-cells display a genetic profile of cytotoxic T-cells. The gene set enrichment analysis revealed a change in 19 processes, including ARF GTPase activator activity; RNA splicing; Signal transduction; Interspecies interaction between organisms; Regulation of ARF GTPase activity; Cell motility; Mitosis; Cell cycle; Anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolic process; Induction of apoptosis by extracellular signals; Negative regulation of apoptosis; mRNA export from nucleus; Positive regulation of ubiquitin-protein ligase activity involved in mitotic cell cycle; Cell division; Protein polymerization; Spliceosome assembly; Microtubule-based movement; Immune response; mRNA processing.
Publication Title
Regulation and gene expression profiling of NKG2D positive human cytomegalovirus-primed CD4+ T-cells.
Sample Metadata Fields
Specimen part
View Samples