GDF5 is a potent tenogenic differentiation inducer. We previously demonstrated that GDF5 induced in vitro tenogenesis of human bone marrow-derived stromal cells (hMSC).
Identification of Pathways Mediating Growth Differentiation Factor5-Induced Tenogenic Differentiation in Human Bone Marrow Stromal Cells.
Specimen part, Subject
View SamplesKnockdowns of c-JUN and JUND had opposite effects on PC3 prostate cell migration. We predicted that c-JUN and JUND control the same set of cell migration genes, but in opposite directions. To test this hypothesis, mRNA with expression changes in c-JUN and JUND knockdown PC3 cell lines were compared to mRNA levels in control (luciferase knockdown) PC3 cells by RNA-seq. Overall design: mRNA profiles of luciferase knockdown (WT), c-Jun knockdown, and Jun-D knockdown in PC3 cells were generated using deep sequencing, in triplicate, using Illumina HiSeq. Knockdowns were stable shRNA expression from a lentiviral construct selected with puromycin.
Extracellular signal-regulated kinase signaling regulates the opposing roles of JUN family transcription factors at ETS/AP-1 sites and in cell migration.
No sample metadata fields
View SamplesWe found that amino acid transporter LHT1 was required for negatively regulating plant defence responses in addition to its physiological role in development and growth. In order to identify which defense pathways were involved in this process, we compared the expression profiles between wild type and lht1 mutant leaves without or with infection by Pseudomonas syringae pv. tomato DC3000 (Pst). In the lht1 mutant, except the changes in nitrogen metabolism-, cellular redox-, and photorespiration-associated gene expressions, the most drastic upregulations were found in the salicylic acid pathway-associated defense genes.
Amino acid homeostasis modulates salicylic acid-associated redox status and defense responses in Arabidopsis.
Specimen part, Treatment
View SamplesTranslocator protein (TSPO), previously known as the peripheral benzodiazepine receptor is a protein of unclear function in the outer mitochondrial membrane. Using TSPO gene-deleted mice, we recently demonstrated that the dogma surrounding mammalian TSPO as a cholesterol transporter essential for steroid hormone production is highly inaccurate. TSPO global knockout mice are apparently healthy and do not have any deficits in steroid hormone production. We present whole transcriptome shotgun sequencing data comparing adrenal gene expression between Tspo floxed (Tspofl/fl) and Tspo knockout (Tspo-/-) mice.
Peripheral benzodiazepine receptor/translocator protein global knock-out mice are viable with no effects on steroid hormone biosynthesis.
No sample metadata fields
View SamplesDiclofenac (DCL) is a non-steroidal anti-inflammatory drug. Its use can be associated with serious adverse drug reactions most notable myocardial infarction and drug-induced liver injury (DILI). The molecular causes leading to DILI remains unclear and it seems to be multifactorial. The aims of this study is to identify the molecular mechanisms involving immune mediated inflammatory reactions and its link to DILI through whole genome gene expression profiling. Diclofenac was given to mice at 30 mg/kg for 1, 3 and 14 days. Microarray experiments were performed with RNA extracts from liver samples. The performed gene expression studies showed >600 significantly regulated genes after single and repeated dosing for 3 and 14 days. The functional annotation revealed several genes were regulated in common coding for inflammatory, immune, stress and acute-phase responses. Immunohistochemistry, qRT-PCR as well as Western blotting were performed to evidence the regulation of key molecules in affected livers. In conclusion, the present study provides evidence for a mechanism of diclofenac induced liver injury that involves pro-inflammatory cytokine and acute phase responses.
Immunogenomics reveal molecular circuits of diclofenac induced liver injury in mice.
Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
EZH2 phosphorylation by JAK3 mediates a switch to noncanonical function in natural killer/T-cell lymphoma.
Disease
View SamplesGene expression profiling of extranodal nasal-type NK/T cell lymphoma and other EBV-associated lymphoid proliferation disease patients was analyzed to elucidate association between JAK-STAT pathway and canonical or non-canonical PRC2/EZH2 target pathways using Illumina HumanRef-8 v3 chips.
EZH2 phosphorylation by JAK3 mediates a switch to noncanonical function in natural killer/T-cell lymphoma.
Disease
View SamplesThe siRNA transfection includes JAK3 and EZH2 siRNAs. The plasmid transfection includes EZH2 WT and its mutants.
EZH2 phosphorylation by JAK3 mediates a switch to noncanonical function in natural killer/T-cell lymphoma.
Cell line
View SamplesGene expression profiling of extranodal nasal-type NK/T cell lymphoma and other EBV-associated lymphoid proliferation disease patients was analyzed to elucidate association between JAK-STAT pathway and canonical or non-canonical PRC2/EZH2 target pathways using Illumina HumanRef-8 v3 chips.
EZH2 phosphorylation by JAK3 mediates a switch to noncanonical function in natural killer/T-cell lymphoma.
Disease
View SamplesSkeletal myogenic commitment of human pluripotent cells can be achieved by doxycycline-inducible expression of the transcription factor PAX7. To gain further insights on PAX7 function during this process, we performed a time course whole transcriptome analysis of differentiating H9 human embryonic stem cells from doxycycline-treated and untreated cultures. In addition, we identified the genomic binding of PAX7 in one of the selected time point (referred as PAX7+ proliferating myogenic progenitors). Overall design: Gene expression profiling was performed on biological replicates from differentiating H9 cells at the following time points: PAX7+ mesodermal cells (day 14), PAX7+ proliferating myogenic progenitors (approximately day 23), and differentiated myocytes (differentiation stage – around day 30; 7 days in the absence of PAX7 induction). Since PAX7 expression is doxycycline inducible, we also collected uninduced control samples at the same time points (termed mesodermal cells for day 14 and proliferating cells for day 23). PAX7 genomic binding was assessed in day 23 dox-treated cultures.
PAX7 Targets, CD54, Integrin α9β1, and SDC2, Allow Isolation of Human ESC/iPSC-Derived Myogenic Progenitors.
No sample metadata fields
View Samples