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SRP125118
Mus musculus
18 Downloadable Samples
Illumina HiSeq 2000
Description
Phenotypic and functional changes seen in the aged adaptive immune system are primarily driven by aging of hematopoietic stem cells (HSCs), pharmacological rejuvenated aged HSCs were able to reconstituted a youthful immune system Overall design: We employed RNA-seq to assess similarities/differences between naive CD4+ T cells and CD19+ B cells isolated from RAG1-/- recipients transplanted with either young, old or old rejuvenated (CASIN treated) HSCs
Publication Title
Aged murine hematopoietic stem cells drive aging-associated immune remodeling.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 32 Downloadable Samples
- Illumina HiSeq 4000
Description
The gene regulatory network in naïve mouse embryonic stem cells (ESCs) must be reconfigured for lineage competence. Tcf3 enables rewiring to formative pluripotency by repressing components of the ESC transcription factor circuitry. However, elimination of Tcf3 only delays, and does not prevent, state transition. Here we delineate distinct contributions of the Ets-family transcription factor Etv5 and the repressor Rbpj. Downstream of Erk1/2 signalling, Etv5 activates enhancers for formative pluripotency. Concomitant up-regulation of Rbpj ensures irreversible exit from the naïve state by extinguishing reversal factors, Nanog and Tbx3. Triple deletion of Etv5, Rbpj and Tcf3 incapacitates ESCs, such that they remain undifferentiated and locked in self-renewal even in the presence of differentiation stimuli. Thus, pluripotency progression is driven hierarchically by two repressors, that respectively dissolve and extinguish the naive network, and an initiator that commissions the formative network. Similar tripartite action may be a general mechanism for efficient cell transitions. Overall design: RNA-seq analysis of parental Rex1-GFPd2 ES cells (RGd2), and deletion mutants generated in this background (Etv5-KO, RbpJ-KO, Etv5-RpbJ-dKO, Etv5-RbpJ-Tcf3-tKO) cultured in 2i, N2B27 or supplemented with Chiron, 3 biological replicates per condition.
Publication Title
Complementary Activity of ETV5, RBPJ, and TCF3 Drives Formative Transition from Naive Pluripotency.
Sample Metadata Fields
Subject
View Samples- Mus musculus
- 633 Downloadable Samples
- Illumina HiSeq 2500
Description
This study explores lineage and regulatory processes involved in early post implantation mouse embryos using single-cell RNA-seq Overall design: Single cells from C57Bl/6Babr mouse embryos at E3.5, E4.5, E5.5 and E6.5 were isolated and subjected to single-cell RNA-seq protocol.
Publication Title
Single-Cell Landscape of Transcriptional Heterogeneity and Cell Fate Decisions during Mouse Early Gastrulation.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 199 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
In chronic lymphocytic leukemia (CLL), 13q14 and 11q22-23 deletions are found in 2/3 of the cases. 11q22-23 deletions are associated with poor survival, whereas 13q14 deletions as single abnormality are often found in indolent disease forms. The molecular basis for this difference in prognosis is not known.
Publication Title
Expression analysis of genes located in the minimally deleted regions of 13q14 and 11q22-23 in chronic lymphocytic leukemia-unexpected expression pattern of the RHO GTPase activator ARHGAP20.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 293 Downloadable Samples
- Illumina HiSeq 2500
Description
Hematopoietic stem cells (HSCs) balance self-renewal and differentiation to maintain homeostasis. With aging, the frequency of polar HSCs decreases. Cell polarity in HSCs is controlled by the activity of the small RhoGTPase Cdc42. Here we demonstrate, using a comprehensive set of paired daughter cell analyses that include single cell 3D-confocal imaging, single cell transplants, single cell RNA-seq as well as single cell ATAC-seq, that the outcome of HSC divisions is strongly linked to the polarity status before mitosis, which is in turn determined by the level of the activity Cdc42 in stem cells. Aged apolar HSCs undergo preferentially self-renewing symmetric divisions, resulting in daughter stem cells with reduced regenerative capacity and lymphoid potential, while young polar HSCs undergo preferentially asymmetric divisions. Mathematical modeling in combination with experimental data implies a mechanistic role of the asymmetric sorting of Cdc42 in determining the potential of daughter cells via epigenetic mechanisms. Therefore, molecules that control HSC polarity might serve as modulators of the mode of stem cell division regulating the potential of daughter cells. Overall design: Sorted single cells were cultured with and without treatment in the presence of cytokines until first cell division (40-44hrs). The daughter cells were manually separated, washed with PBS and collected for RNA sequencing.
Publication Title
Aging alters the epigenetic asymmetry of HSC division.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
In this experiments different treatments were applied to lung cancer cell lines
Publication Title
Ingenuity network-assisted transcription profiling: Identification of a new pharmacologic mechanism for MK886.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 194 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Chronic lymphocytic leukemia (CLL) is a common and heterogeneous disease. An accurate prediction of outcome is highly relevant for the development of personalized treatment strategies. Microarray technology was shown to be a useful tool for the development of prognostic gene expression scores. However, there are no gene expression scores which are able to predict overall survival in CLL based on the expression of few genes that are better than established prognostic markers. We correlated 151 CLL microarray data sets with overall survival using Cox regression and supervised principal component analysis to derive a prognostic score. This score based on the expression levels of eight genes and was validated in an independent group of 149 CLL patients by quantitative real time PCR. The score was predictive for overall survival and time to treatment in univariate Cox regression in the validation data set (both: p<0.001) and in a multivariate analysis after adjustment for 17p and 11q deletions and the IgVH-status. The score achieved superior prognostic accuracy compared to models based on genomic aberrations and IgVH-status and may support personalized therapy.
Publication Title
An eight-gene expression signature for the prediction of survival and time to treatment in chronic lymphocytic leukemia.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Rattus norvegicus
- 15 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
Neuronal differentiation of PC12 cells in response to NGF is a prototypical model in which signal duration determines a biological response. Sustained ERK activity induced by NGF, as compared to transient activity induced by EGF, is critical to the differentiation of these cells. To characterize the transcriptional program activated preferentially by NGF, we compared global gene expression profiles between cells treated with NGF and EGF for 2-4 hrs, when sustained ERK signaling in response to NGF is most distinct from the transient signal elicited by EGF. This analysis identified 69 genes that were preferentially upregulated in response to NGF.
Publication Title
Global expression analysis identified a preferentially nerve growth factor-induced transcriptional program regulated by sustained mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) and AP-1 protein activation during PC12 cell differentiation.
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We propose the hypothesis that loss of estrogen receptor function which leads to endocrine resistance in breast cancer, also results in de-differentiation from an epithelial to a mesenchymal phenotype that is responsible for increased aggressiveness and metastatic propensity. siRNA mediated silencing of the estrogen receptor in MCF7 breast cancer cells resulted in estrogen/tamoxifen resistant cells (pII) with altered morphology, increased motility with rearrangement and switch from an actin to a vimentin based cytoskeleton, and ability to invade simulated components of the extracellular matrix. Phenotypic profiling using an Affymetrix Human Genome U133 plus 2.0 GeneChip indicated fold changes 3 in approximately 2500 identifiable unique sequences, with about 1270 of these being up-regulated in pII cells. Changes were associated with genes whose products are involved in cell motility, loss of cellular adhesion and interaction with the extracellular matrix. Selective analysis of the data also showed a shift from luminal to basal cell markers and increased expression of a wide spectrum of genes normally associated with mesenchymal characteristics, with consequent loss of epithelial specific markers. Over-expression of several peptide growth factors and their receptors are indicative of an increased contribution to the higher proliferative rates of pII cells as well as aiding their potential for metastatic activity. Signalling molecules that have been identified as key transcriptional drivers of epithelial to mesenchymal transition were also found to be elevated in pII cells. We suggest that these data support our hypothesis that induced loss of estrogen receptor in previously antiestrogen sensitive cells is a trigger for the concomitant loss of endocrine dependence and onset of a series of possibly parallel events that changes the cell from an epithelial to a mesenchymal type. Inhibition of this transition through targeting of specific mediators may be a useful supplementary strategy to circumvent the effects of loss of endocrine sensitivity.
Publication Title
Estrogen receptor silencing induces epithelial to mesenchymal transition in human breast cancer cells.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Ischaemic preconditioning is a method of protecting tissue against ischaemia-reperfusion injury. It is an innate protective mechanism that increases a tissue's tolerance to prolonged ischaemia when it is first subjected to short burst of ischaemia and reperfusion. It is thought to provide this protection by increasing the tissue's tolerance to ischaemia, therby reducing oxidative stress, inflammation and apoptosis in the preconditioned tissue.
Publication Title
Transcriptional responses in the adaptation to ischaemia-reperfusion injury: a study of the effect of ischaemic preconditioning in total knee arthroplasty patients.
Sample Metadata Fields
Specimen part, Time
View Samples