Hematopoietic Stem Cells (HSC) are originated during embryonic development from endothelial-like cells located in the ventral side of the dorsal aorta around day E10-12 of murine development. This region is called AGM for Aorta/Gonad/Mesonephros refering to the tissues around the hemogenic aorta. Cells that emerge from the endothelium and show hematopoietic traits can be distinguished by the expression of the c-kit receptor and finally acquire the CD45 marker. The effect of Notch activation by each one of the ligands has been tested on c-kit+ and ckit- cells from the endothelium of the E11.5 AGM . Incubations with stromal cell lines exposed the cells to high levels of ligand and induced changes in the transcriptome of these cells.
No associated publication
Specimen part
View SamplesGene expression from MCF7 breast cancer cells at different times of TNFa incubation:pcs2 and 14-3-3 transduced cells
Inhibition of specific NF-κB activity contributes to the tumor suppressor function of 14-3-3σ in breast cancer.
Time
View SamplesHematopoietic Stem Cells (HSC) are originated during embryonic development from endothelial-like cells located in the ventral side of the dorsal aorta around day E10-12 of murine development. This region is called AGM for Aorta/Gonad/Mesonephros and refers to the tissues around the hemogenic aorta. Cells that emerge from the endothelium and show hematopoietic traits can be distinguished by the expression of the c-kit receptor and finally acquire the CD45 marker.
Hematopoietic stem cell development requires transient Wnt/β-catenin activity.
Specimen part
View SamplesImmunoglobulin A (IgA) is the most abundant antibody in the intestinal tract. Recent studies show that discrete subsets of gut human plasma cells (PCs) release IgA, which contributes to the maintenance of gut homeostasis. To better characterize the properties of these PC subsets, we performed global transcriptome analysis in naïve B cells as well as immature CD19+IgA+CD138- PCs, mature CD19+IgA+CD138+ PCs and late CD19-IgA+CD138+ PCs after their purification from human colon samples.
No associated publication
Specimen part, Subject
View SamplesH69M cells derive from H69 small cell lung cancer cells subjected to prolonged treatment with HGF. Among the whole population of cells, a subset of more fibroblastic cells was isolated (H69M-mesenchymal). In this experiment we compared expression profiles of both cell lines
Targeting epithelial-to-mesenchymal transition with Met inhibitors reverts chemoresistance in small cell lung cancer.
Specimen part, Cell line
View SamplesBackground: Interval breast cancers can occur through failure to detect an abnormality at the time of screening (missed interval cancer), or as a new event after a negative screen (true interval cancer). The development and progression of true interval tumors (TIBC) is known to be different than screen-detected tumors (SDBC). However, much work still needs to be done to understand the biological characteristics and clinical behaviour of these TIBC. Objectives: To characterize the gene expression profile in TIBC and SDBC aimed to identify biological markers that may be associated with the emergence of symptomatic breast cancer in the screening interval. Material and Methods: An unsupervised exploratory gene expression profile analysis was performed among 10 samples (discovery set, TIBC=5 and SDBC=5) using Affymetrix Human Gene 1.0 ST arrays and interpreted by Ingenuity Pathway Analysis. Differential expression of selected genes was confirmed in validation series of 91 patients (TIBC=12 and SDBC=79) by immunohistochemistry and 24 patients (TIBC=8 and SDBC=16) by RT-qPCR, expanding the analysis to other genes in same pathway (mTOR, 4E-BP1, eIF-4G and S6).
Gene expression profiling in true interval breast cancer reveals overactivation of the mTOR signaling pathway.
Specimen part
View SamplesAlthough heterochromatin is enriched with repressive traits, it is also actively transcribed, giving rise to large amounts of non-coding RNAs. Although these RNAs are responsible for the formation and maintenance of heterochromatin, little is known about how their transcription is regulated. Here we show that the Snail1 transcription factor represses pericentromeric transcription, acting through the H3K4 deaminase LOXL2. Since Snail1 plays a key role in the epithelial to mesenchymal transition (EMT), we analyzed the regulation of mouse heterochromatin transcription in this process. At the onset of EMT, one of the major structural heterochromatin proteins, HP1a, is transiently released from heterochromatin foci in a Snail1/LOXL2dependent manner during EMT, concomitantly with a down-regulation of major satellite transcription. Global transcriptome analysis indicated that ectopic expression of heterochromatin transcripts affects the transcription profile of EMT-related genes. Additionally, preventing the down-regulation of major satellite transcripts compromised the migratory and invasive behavior of mesenchymal cells. We propose that Snail1 regulates heterochromatin transcription through the histone-modifying enzyme, LOXL2, thus creating the favorable transcriptional state necessary for completing EMT.
Regulation of heterochromatin transcription by Snail1/LOXL2 during epithelial-to-mesenchymal transition.
Cell line, Treatment
View SamplesGene expression from MDA-MB-231 cells shControl and shLOXL2.
Lysyl oxidase-like 2 (LOXL2) oxidizes trimethylated lysine 4 in histone H3.
Cell line
View SamplesPrimary T cells were isolated from spleen of Parp-1-/- and wild-type mice by magnetic depletion of non-T cells using a MACS Pan-T Cell isolation kit, according to the manufacturer´s instruction (Mintenyi Biotec, Bergisch Gladbach, Germany). Purity was assessed by flow cytometry analysis using antibodies against CD3, CD4 and CD8 and all preparations were more than 98% pure of T cells. The cells were activated with plate-bound anti-mouse CD3 (clone 145-2C11) (5 microg/ml) in the absence or the presence of anti-mouse CD28 (clone 37.51) (5microg/ml) both from BD PharMingen (San Diego, CA) and culture for 3.5 h in RPMI 1640 medium (BioWhittaker) supplemented with 10% FCS, 2mM L-glutamine, 5x10-5 M 2-mercaptoethanol (Sigma), 2.5 microg/ml fungizone, 100 IU/ml penicillin, and 10 microg/ml streptomycin.
Transcriptional regulation by poly(ADP-ribose) polymerase-1 during T cell activation.
Age, Specimen part
View SamplesTranscriptional dysregulation in Huntingtons disease (HD) is an early event that affects the expression of genes involved in survival and neuronal functions throughout the progression of the pathology. In the last years, extensive research has focused on epigenetic and chromatin-modifying factors as a causative explanation for such dysregulation, offering attractive targets for pharmacological therapies. In this work we examined the gene expression profiles in cortex, striatum, hippocampus and cerebellum of juvenile R6/1 and N171-82Q mice, two models of fast progressive HD, to retrieve the early transcriptional signatures associated with this pathology.These profiles showed significant coincidences with the transcriptional changes in the conditional knockout for the lysine acetyltransferase CBP in postmitotic forebrain neurons.
Early alteration of epigenetic-related transcription in Huntington's disease mouse models.
Sex, Age, Specimen part
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