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Homo sapiens
25 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
This work focuses on understanding the molecular basis of the immune dysfunctions in Idiopathic CD4+ T cells lymphocytopenia (ICL). ICL is a rare haematological disorder of unknown origin, characterized by a profound and persistent CD4+ T-cell defect, which predisposes to life threatening opportunistic infections very similar to those seen in AIDS. To analyse more in depth the functional pathways involved in ICL pathogenesis, we conducted gene expression profiling of CD4+ T-cells isolated from blood samples from ICL, sarcoidosis and healthy individuals. Our analyses have revealed specific CD4+ T-cells gene expression signatures in ICL associated with defective TCR activation threshold, expansion of the Treg-cell compartment and interestingly with accelerated immune aging.
Publication Title
DUSP4-mediated accelerated T-cell senescence in idiopathic CD4 lymphopenia.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 74 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cyclophilin binding drugs, NIM811 and cyclosporin A (CsA), inhibit the replication of HCV replicon.
Publication Title
Multiple cyclophilins involved in different cellular pathways mediate HCV replication.
Sample Metadata Fields
Time
View Samples- Mus musculus
- 12 Downloadable Samples
Illumina HiSeq 2500
Description
Purpose: In our study, we identified a heterogeneity among bone marrow (BM) Ly6Chi monocytes, which can be subdivided the expression of CXCR4. In order to understand the development of BM monocytes, the goal of this experiment is to compare the transcriptome of these 2 BM Ly6Chi monocyte subsets to those of the common monocyte progenitor (cMoP) and Ly6Clo monocytes. Overall design: 4 BM monocyte subsets (cMoP, Ly6ChiCXCR4hi, Ly6ChiCXCR4lo and Ly6Clo) from 3 different mice were sorted using a BD Aria III. Total RNA was extracted, converted to cDNA and run through deep sequencing using Illumina HiSeq 2500
Publication Title
CXCR4 identifies transitional bone marrow premonocytes that replenish the mature monocyte pool for peripheral responses.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 14 Downloadable Samples
- Illumina HiSeq 2500
Description
Our study aims to analyze time-dependent changes in neutrophil phenotype, compare them with included neutrophil-specific mutants, and indentify common signatures among the 5 groups Overall design: Blood neutrophils from wild-type and mutants were isolated based on Ly6G staining, then standard RNA extraction procedures were performed. Wild-type samples were extracted at ZT5 and ZT13, all other samples at ZT5.
Publication Title
A Neutrophil Timer Coordinates Immune Defense and Vascular Protection.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina HiSeq 2500
Description
Our study aims to analyze time-dependent changes in neutrophil phenotype Overall design: Blood neutrophils were isolated based on Ly6G staining, then standard RNA extraction procedures were performed. This samples were extracted at ZT13.
Publication Title
A Neutrophil Timer Coordinates Immune Defense and Vascular Protection.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Biallelic inactivating mutations of the transcription factor 1 gene (TCF1), encoding hepatocyte nuclear factor 1a (HNF1a), were identified in 50% of hepatocellular adenomas (HCA) phenotypically characterized by a striking steatosis. To understand the molecular basis of this aberrant lipid storage, we performed a microarray transcriptome analysis validated by quantitative RT-PCR, western-blotting and lipid profiling. In mutated HCA, we showed a repression of gluconeogenesis coordinated with an activation of glycolysis, citrate shuttle and fatty acid synthesis predicting elevated rates of lipogenesis. Moreover, the strong dowregulation of L-FABP suggests that impaired fatty acid trafficking may also contribute to the fatty phenotype. In addition, transcriptional profile analysis of the observed deregulated genes in non-HNF1a-mutated HCA as well as in non-tumor livers allowed us to define a specific signature of the HNF1a-mutated HCA. In theses tumors, lipid composition was dramatically modified according to the transcriptional deregulations identified in the fatty acid synthetic pathway. Surprisingly, lipogenesis activation did not operate through SREBP-1 and ChREBP that were repressed. We conclude that steatosis in HNF1a-mutated HCA results mainly from an aberrant promotion of lipogenesis that is linked to HNF1a inactivation and that is independent of both SREBP-1 and ChREBP activation. Finally, our findings have potential clinical implications since lipogenesis can be efficiently inhibited by targeted therapies.
Publication Title
HNF1alpha inactivation promotes lipogenesis in human hepatocellular adenoma independently of SREBP-1 and carbohydrate-response element-binding protein (ChREBP) activation.
Sample Metadata Fields
Sex, Specimen part, Disease
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Focal nodular hyperplasias (FNHs) are benign liver lesions considered to be a hyperplastic response to increased blood flow in otherwise normal liver. In contrast, FNH-like nodules occur in cirrhotic liver but share similar histopathological features. To better understand the pathophysiology of FNH, we performed a transcriptomic analysis. Methods: Affymetrix and cDNA microarrays were used to compare gene expression in eight FNHs with that in tissue from six normal livers. Selected genes were validated with quantitative RT-PCR in 70 benign liver tumors including adenomas and cirrhotic and FNH-like lesions. Results: Among the deregulated genes in FNHs, 19 were physiologically zonated in the normal liver lobule. All six periveinous genes were up-regulated in FNH, whereas 13 genes normally expressed in the periportal area were down-regulated. Immunohistochemistry revealed that glutamine synthetase was markedly overexpressed, forming anastomosed areas usually centered on visible veins. -catenin mRNA was slightly but significantly overexpressed, as were several known -catenin target genes. Moreover, activated hypophosphorylated -catenin protein accumulated in FNH in the absence of activating mutations. These results suggest zonated activation of the -catenin pathway specifically in FNH, whereas the other benign hepatocellular tumors, including FNH-like lesions, demonstrated an entirely different pattern of -catenin expression. Conclusions: In FNH, increased expression of the -catenin pathway was restricted to enlarged periveinous areas, which may explain the slight polyclonal over-proliferation of hepatocytes at the origin of the lesion. FNH-like nodules may have a different pathogenetic origin.
Publication Title
The beta-catenin pathway is activated in focal nodular hyperplasia but not in cirrhotic FNH-like nodules.
Sample Metadata Fields
Sex, Specimen part, Disease
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Inflammatory hepatocellular adenomas (IHCA) are benign liver tumours defined by the presence of inflammatory infiltrates and by the elevated expression of inflammatory proteins in tumour hepatocytes1,2. Here we show a striking activation of the IL6 signalling pathway in this tumour type, and sequencing candidate genes pinpointed this response to somatic gain-of-function mutations in the IL6ST gene that encodes the signalling co-receptor gp130. Indeed, ~70% of IHCA harbour small in-frame deletions that target the binding site of gp130 for IL6, and expression of the most frequent gp130 mutant, Delta-STVY190, in hepatocellular cells activates STAT3 in absence of ligand. Further, analysis of hepatocellular carcinomas revealed rare gp130 alterations always accompanied by -catenin-activating mutations, suggesting a cooperative effect of these signalling pathways in the malignant conversion of hepatocytes. The recurrent gain-of-function gp130 mutations in these human hepatocellular adenomas explains their inflammatory phenotype, and suggest that similar alterations may occur in other inflammatory epithelial tumours with STAT3 activation.
Publication Title
Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumours.
Sample Metadata Fields
Sex, Specimen part, Disease
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Neuronal, endocrine and exocrine cells exhibit regulated exocytosis but there is also a body of evidence for regulated exocytosis from other cell types. Myofibroblasts are a stromal cell type that secretes extracellular matrix proteins, growth factors and cytokines; they are important in wound healing and increasingly are recognised to play a role in modifying the cellular microenvironment in cancer. We have established calcium dependent regulated secretion in a subset of myofibroblasts from gastric cancers, adjacent tissue and from normal tissue. We have used microarrays to look for the expression of genes associated with the regulated secretory phenotype.
Publication Title
The neuroendocrine phenotype of gastric myofibroblasts and its loss with cancer progression.
Sample Metadata Fields
Specimen part
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GSE38961- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The Loeys-Dietz syndrome (LDS) is an inherited connective tissue disorder caused by mutations in the transforming growth factor (TGF-) receptors TGFBR1 or TGFBR2. Most patients with LDS develop severe aortic aneurysms resulting in early need of surgical intervention. We investigated circulating outgrowth endothelial cells (OEC) from the peripheral blood of LDS to gain further insight into the pathophysiology of the disorder. We performed gene expression profiling using microarray analysis followed by quantitative PCR for verification of gene expression. OECs isolated from age- and sex-matched healthy donors served as reference control.
Publication Title
Overexpression of Gremlin-1 in patients with Loeys-Dietz syndrome: implications on pathophysiology and early disease detection.
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples