This study compared the gene expression change of glioblastoma stem-like cells before and after retinoic acid treatment
Regulation of glioblastoma stem cells by retinoic acid: role for Notch pathway inhibition.
Specimen part, Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Metabolomic Identification of Subtypes of Nonalcoholic Steatohepatitis.
Age, Specimen part, Treatment
View SamplesMethionine adenosyltransferase (MAT) enzymes generate SAMe (S-adenosylmethionine), the main biological methyl donor. There are two MAT encoding genes in mammals (Mat1a and Mat2a), which show different activities and cellular distribution. Mat1a encodes the enzyme mainly expressed in normal liver. Mat1a ablation in mice results in the spontaneous development of non-alcoholic steatohepatitis (NASH). We observed that SAMe depletion in Mat1a KO mice had three main effects on hepatic lipid metabolism: 1) impaired TG (triglyceride) export via VLDL; 2) impaired mitochondrial FA (fatty acid) oxidation (as evidenced by membrane depolarization, downregulation of Phb1 (prohibitin 1, a mitochondrial chaperone protein) and Mcj/Dnajc15 (endogenous mitochondrial repressor of respiratory chain), and accumulation of long-chain acylcarnitines); and 3) increased FA uptake. The convergence of these three factors induced TG accumulation in LD (lipid droplets). LD expansion confronts hepatocytes with a high demand of PC (phosphatidylcholine) molecules to cover the LD surface since other phospholipids, such as PE (phosphatidylethanolamine), cannot stabilize LD and prevent coalescence. In Mat1a KO this situation is aggravated, since SAMe-dependent PC synthesis via PE methylation is decreased, the PC/PE ratio reduced and mitochondrial FA oxidation impaired. To put a brake to this drain of PC molecules to LD, FA are rerouted in Mat1a KO mice liver to other catabolic (endoplasmic reticulum and peroxisome oxidation) and biosynthetic (ceramides synthesis) pathways, causing oxidative stress, inflammation and fibrosis. SAMe treatment for two months in 8-9 month old Mat1a KO mice ameliorated mitochondrial dysfunction (reduces membrane depolarization, improves Phb1 and Mcj expression, and increases SAMe transport to mitochondria) improving FA oxidation efficiency (FA and acylcarnitine levels decrease), which results in a drastic reduction in TG accumulation. SAMe treatment in Mat1a KO mice resulted in more PC available for proper membrane function, improving liver lipid homeostasis, histology (H&E, Sudan red, Sirius red) and liver injury (ALT, AST).
Metabolomic Identification of Subtypes of Nonalcoholic Steatohepatitis.
Age, Specimen part
View SamplesWe had evidence that TRIM5 regulates signal transduction, specifically NFkB and MAPK pathways. To test the role of endogenous TRIM5 we used the myelomonocytic leukemia cell line THP1. These cells were transduced with a lentiviral vector that delivers a miRNA engineered to knockdown TRIM5. The vector also encoded a puromycin-resistance cassette and transduced cells were selected in poold with puromycin. As a control, cells were transduced with a vector targeting luciferase instead of TRIM5.
TRIM5 is an innate immune sensor for the retrovirus capsid lattice.
Specimen part, Cell line
View SamplesCdk4/6 inhibitors have shown to increase overall survival in hormone-positive breast tumors, but whether other solid tumors could respond to these inhibitors has not yet defined. Here we show that Palbociclib (a Cdk4/6 specific inhibitor in clinic use) treatment exerts antiproliferative effects in vivo using a bladder cancer cell lines.
CDK4/6 Inhibitor as a Novel Therapeutic Approach for Advanced Bladder Cancer Independently of <i>RB1</i> Status.
Specimen part, Cell line
View SamplesWe are reporting here the effects of adaptation to different ambient temperatures in the whole genome gene expression of interscapular BAT of BAT specific Akt2 knockout mice Overall design: Wildtype littermates and brown fat specific Akt2 KO mice (using UCP1-CreER) in B6/J background were adapted to 2 different ambient temperatures (30ºC, 22ºC) for a period of 4 weeks.
Brown Fat AKT2 Is a Cold-Induced Kinase that Stimulates ChREBP-Mediated De Novo Lipogenesis to Optimize Fuel Storage and Thermogenesis.
Age, Specimen part, Cell line, Treatment, Subject
View SamplesWe are reporting here the effects of adaptation to different ambient temperatures in the whole genome gene expression of interscapular BAT Overall design: B6/J mice were adapted to three different ambient temperatures (30ºC, 22ºC and 6ºC) for a period of 4 weeks.
Brown Fat AKT2 Is a Cold-Induced Kinase that Stimulates ChREBP-Mediated De Novo Lipogenesis to Optimize Fuel Storage and Thermogenesis.
Age, Specimen part, Cell line, Treatment, Subject
View SamplesThe human C-type lectin Reg3a (HIP/PAP) is an antimicrobial peptide that kills Gram-positive bacteria. Reg3a preserves gut microbiota homeostasis, reinforces intestinal barrier function and thereby helps to fight induced colitis in mice.
Enteric Delivery of Regenerating Family Member 3 alpha Alters the Intestinal Microbiota and Controls Inflammation in Mice With Colitis.
Specimen part, Treatment
View SamplesAnxA4 expression is increased in H. pylori associated tumors. Moreover, in renal-cell cancer, AnxA4 increases tumor cell dissemination and promotes cell migration, and in colorectal cancer, it is identified as a potential diagnostic marker. How AnxA4 might be involved in tumorgenesis has remained unclear.
Revealing the molecular mechanism of gastric cancer marker annexin A4 in cancer cell proliferation using exon arrays.
Cell line, Treatment
View SamplesAllergic diseases correspond to a broad range of hypersensitivity reactions, often occurring as co-morbidities. Investigation of the molecular basis of allergy is a challenge because of its highly heterogeneous nature. We combined large-scale and high-throughput gene expression technology and systems biology approaches to retrieve relevant biomarkers and signalling pathways.
A novel whole blood gene expression signature for asthma, dermatitis, and rhinitis multimorbidity in children and adolescents.
Sex, Age, Specimen part
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