This study was performed to investigate the effect of IL-37 on the transcriptional profile of eosinophils upon co-culture with human bronchial epithelial BEAS-2B cells and peptidoglycan (PGN) stimulation.
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Sex, Specimen part, Disease, Treatment
View SamplesTranscriptome seqeunecing on 16 paired HCCs and non-tumorous livers to investigate the effect of HBV integration
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View Samplesold and young human cardiac fibroblasts plus those treated with rapamycin and methionine restriction or a combination of both
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Sex, Specimen part
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View SamplesPTEN encodes a lipid phosphatase that is underexpressed in many cancers owing to deletions, mutations or gene silencing. PTEN dephosphorylates phosphatidylinositol 3,4,5-triphosphate (PIP3), thereby opposing the activity of class I phosphatidylinositol 3-kinases (PI3Ks) that mediate growth and survival factors signaling through PI3K effectors such as AKT and mTOR. To determine whether continued PTEN inactivation is required to maintain malignancy, we generated an RNAi-based transgenic mouse model that allows tetracycline-dependent regulation of PTEN in a time- and tissue-specific manner. Postnatal PTEN knockdown in the hematopoietic compartment produced highly disseminated T-cell leukemia (T-ALL). Surprisingly, reactivation of PTEN mainly reduced T-ALL dissemination but had little effect on tumor load in hematopoietic organs. Lymphoma infiltration into the intestine was dependent on CCR9 G-protein coupled receptor (GPCR) signaling, which was amplified by PTEN loss. Our results suggest that in the absence of PTEN, GPCRs may play an unanticipated role in driving tumor growth and invasion in an unsupportive environment. They further reveal that the role of PTEN loss in tumor maintenance is not invariant and can be influenced by the tissue microenvironment, thereby producing a form of intratumoral heterogeneity that is independent of cancer genotype.
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View SamplesObesity, an immense epidemic affecting approximately half a billion adults, has doubled in prevalence in the last several decades. Epidemiological data support that obesity due to intake of a high-fat, western diet increases the risk of colon cancer; however, the mechanisms underlying this risk remain unclear. Here, utilizing next generation RNA sequencing, we aimed to determine the high-fat diet mediated gene expression profile in mouse colon and the AOM/DSS model of colon cancer.
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Sex, Specimen part, Disease, Cell line, Treatment
View SamplesHOX A13 over expression represents: i) a novel molecular marker of hepatocellular carcinomas; ii) a sign of epithelial-endothelial transition accounting for tumor independent angiogenesis and lymphangiogenesis.
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View SamplesTo identify the putative mechanisms of action of MCAM, we performed RNA-sequencing to define the transcriptional changes induced by MCAM knockdown. A biological triplicate for MCAM knockdown cells and control samples (shRNA-NT) was generated and total RNA extracted for RNA sequencing.
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Sex, Specimen part, Disease, Cell line
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View SamplesNonsense-mediated mRNA decay (NMD) surveillance pathways are best known to be involved in the degradation of mRNA with premature termination codons (PTCs). More recent studies demonstrate that the role of NMD pathways goes well beyond the degradation of PTC containing mRNA, into the regulation of cell function and thus normal development.
Transcriptome profiling of UPF3B/NMD-deficient lymphoblastoid cells from patients with various forms of intellectual disability.
Specimen part, Disease, Disease stage, Cell line, Subject
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