T cell development relies on the precise developmental control of various cellular functions for appropriate positive and negative selection. Previously, gene expression profiling of peptide-driven negative selection events in the N15 TCR class I MHC-restricted mouse and D011.10 TCR class II MHC-restricted mouse has offered insights into the coordinate engagement of biological processes affecting thymocyte development. However, there has been little comparable detailed in vivo global genome expression analysis reported for positive selection.
PlexinD1 glycoprotein controls migration of positively selected thymocytes into the medulla.
No sample metadata fields
View SamplesThe original objectives of the study were to identify surface markers specifically expressed in motor neurons. We now use the data to profile the expression of Cdk family members in motor neurons.
Dual Inhibition of GSK3β and CDK5 Protects the Cytoskeleton of Neurons from Neuroinflammatory-Mediated Degeneration In Vitro and In Vivo.
Specimen part
View SamplesEndogenous oligodendrocyte progenitor cells (OPCs) are a promising target to improve functional recovery after spinal cord injury (SCI) by remyelinating denuded, and therefore vulnerable, axons. Demyelination is the result of a primary insult and secondary injury, leading to conduction blocks and long-term degeneration of the axons, which subsequently can lead to the loss of their neuron. In response to SCI, dormant OPCs can be activated and subsequently start to proliferate and differentiate into mature myelinating oligodendrocytes (OLs). Therefore, researchers strive to control OPC responses, and utilize small molecule screening approaches in order to identify mechanisms of OPC activation, proliferation, migration and differentiation. Overall design: DEG analysis of primary OPC and OL populations, 5 biological replicates per population
Primary Spinal OPC Culture System from Adult Zebrafish to Study Oligodendrocyte Differentiation <i>In Vitro</i>.
No sample metadata fields
View SamplesComparison between cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel
Multifactorial regulation of E-cadherin expression: an integrative study.
Sex, Age, Specimen part, Disease, Disease stage, Cell line, Time
View SamplesBACKGROUND: Climate change will lead in the future to an occurrence of heat waves with a higher frequency and duration than observed today, which has the potential to cause severe damage to seedlings of temperate maize genotypes. In this study, we aimed to (I) assess phenotypic variation for heat tolerance of temperate European Flint and Dent maize inbred lines, (II) investigate the transcriptomic response of temperate maize to linearly increasing heat levels and, (III) identify genes associated with heat tolerance in a set of genotypes with contrasting heat tolerance behaviour. RESULTS: Strong phenotypic differences with respect to heat tolerance were observed between the examined maize inbred lines on a multi-trait level. We identified 607 heat responsive genes as well as 39 heat tolerance genes. CONCLUSION: Our findings indicate that individual inbred lines developed different genetic mechanisms in response to heat stress. We applied a novel statistical approach enabling the integration of multiple genotypes and stress levels in the analysis of abiotic stress expression studies. Overall design: Identifcation of differentially expressed genes between 8 genotypes and 3 heat levels
Genome-wide expression profiling and phenotypic evaluation of European maize inbreds at seedling stage in response to heat stress.
Specimen part, Subject
View SamplesThe purpose of this study was to determine whether the serum condition affected the gene expression in mesenchymal stem cells (MSCs)over time. To that end, we compared gene expression in MSCs maintained in regular growth medium supplemented with fetal calf serum (FCS) for 10 passages with gene expression of MSCs cultured in the same conditions for 4 passages for 2 different donors (i.e. donor3 and donor4). Likewise, we compared gene expression in MSCs maintained in regular growth medium supplemented with autologous serum(AS) for 10 passages with gene expression of MSCs cultured in the same conditions for 4 passages for the same 2 donors (i.e. donor3 and donor4). MSCs were cultured in FCS- or AS-supplemented medium and were analyzed at passage 4 and at passage 10.
In vitro expansion of human mesenchymal stem cells: choice of serum is a determinant of cell proliferation, differentiation, gene expression, and transcriptome stability.
Sex, Specimen part, Subject
View SamplesThe purpose of this study was to determine whether the serum condition affected the gene expression in mesenchymal stem cells (MSCs). To that end, we compared gene expression in MSCs maintained in regular growth medium supplemented with fetal calf serum (FCS) with gene expression of MSCs cultured in regular growth medium supplemented with autologous serum (AS) for 3 different donors (i.e. donor2, donor3 and donor4). MSCs were cultured in FCS- or AS-supplemented medium and were analyzed at passage 4.
In vitro expansion of human mesenchymal stem cells: choice of serum is a determinant of cell proliferation, differentiation, gene expression, and transcriptome stability.
Sex, Specimen part, Subject
View SamplesOne of the most common genetic alterations in acute myeloid leukemia is the internal tandem duplication (ITD) in the FLT3 receptor for cytokine FLT3 ligand (FLT3L). The constitutively active FLT3-ITD promotes the expansion of transformed progenitors, but also has pleiotropic effects on normal hematopoiesis. We analyzed the effect of FLT3-ITD on dendritic cells (DCs), which express FLT3 and can be expanded by FLT3L administration. We report that young pre-leukemic mice with the Flt3ITD knock-in allele manifest an expansion of all DCs including classical (cDCs) and plasmacytoid (pDCs). The expansion originated in DC progenitors, occurred in a cell-intrinsic manner and was further enhanced in Flt3ITD/ITD mice. The mutation caused the downregulation of Flt3 on the surface of DCs and reduced their responsiveness to Flt3L. Flt3ITD mice showed enhanced capacity to support T cell proliferation, including a cell-extrinsic expansion of regulatory T cells (Tregs). Accordingly, these mice restricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoimmunity in the absence of Tregs. Thus, the FLT3-ITD mutation directly affects DC development, thereby indirectly modulating T cell homeostasis and supporting Treg expansion. This effect of FLT3-ITD may subvert immunosurveillance and promote leukemogenesis in a cell-extrinsic manner. Overall design: Sorted splenic dendritic cell subsets from either Flt3+/+ or Flt3ITD/+ mice were sequenced for mRNA profiling. For each subset per genotype contains 2-3 replicates, all from independent experiments.
Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses.
Specimen part, Cell line, Subject
View SamplesSTEP (striatal-enriched tyrosine phosphatase) is a brain-specific phosphatase named for its robust expression in striatum. Brains from homozygous and heterozygous STEP knockout mice and wild-type littermates were harvested, and striatum microdissected. RNA was extracted and hybridized to Affymetrix 230_2 microarray chips.
Downstream effects of striatal-enriched protein tyrosine phosphatase reduction on RNA expression in vivo and in vitro.
Sex, Specimen part, Treatment
View SamplesSignal transducer and activator of transcription 3 (STAT3) is altered in several epithelial cancers and represents a potential therapeutic target. Here, STAT3 expression, activity and cellular functions were examined in two main histotypes of esophageal carcinomas. In situ, immunohistochemistry for STAT3 and STAT3-Tyr705 phosphorylation (P-STAT3) in esophageal squamous cell carcinomas (ESCC) and Barretts adenocarcinomas (BAC) revealed similar STAT3 expression in ESCCs and BACs, but preferentially activated P-STAT3 in ESCCs. In vitro, strong STAT3 activation was seen by EGF-stimulation in OE21 (ESCC) cells, whilst OE33 (BAC) cells showed constitutive weak STAT3 activation. STAT3 knockdown significantly reduced cell proliferation of OE21 and OE33 cells and reduced cell migration in OE33, but not in OE21 cells. Transcriptome analysis identified STAT3-knockdown associated down-regulation of cell cycle processes and the selective down-regulation of cyclins and cyclin dependent kinaes associated genes in both OE21 and OE33 cells. Moreover, the transcriptome response showed changes in cell migration/invasion related genes that correlated with the associated phenotype measurements. This study demonstrates the importance of STAT3 expression and activation in esophageal carcinomas, whereby the extent differs between ESCCs and BACs. STAT3 knockdown significantly reduces cell proliferation in both types of esophageal cancer cells and inhibits migration in BAC cells. Thus, STAT3 may be further exploited as potential novel therapeutic target for esophageal cancers.
STAT3 expression, activity and functional consequences of STAT3 inhibition in esophageal squamous cell carcinomas and Barrett's adenocarcinomas.
Cell line, Treatment
View Samples