Hematopoietic stem cell (HSC) are regulated by their niche, which limits activation of HSCs, to ensure their maintenance and self-renewal.
Stroma-Derived Connective Tissue Growth Factor Maintains Cell Cycle Progression and Repopulation Activity of Hematopoietic Stem Cells In Vitro.
Cell line
View SamplesDAP12 is a transmembrane protein, expressed as a disulfide-bonded homodimer and bears an immunoreceptor tyrosine-based activation motif (ITAM). DAP12 is broadly expressed in hematopoietic cells and associates with a variety of cell surface receptors in lymphoid and myeloid cells. Macrophages express several DAP12-associated receptors including triggering receptors expressed by myeloid cells (TREM)-1,2 and 3, myeloid DAP12-associating lectin (MDL)-1, CD200R like proteins CD200R3/R4 and CD300C/D/E .
Essential role of DAP12 signaling in macrophage programming into a fusion-competent state.
No sample metadata fields
View SamplesExpression analysis of mature Arabidopsis trichomes in Col-0 and two mutants, triptychon (try-JC) and glabra3 (gl3-3)
Transcriptional profiling of mature Arabidopsis trichomes reveals that NOECK encodes the MIXTA-like transcriptional regulator MYB106.
Specimen part
View SamplesTranscription profiling by array of pancreas from KrasG12D, Ela-Tgfa and KrasG12D Ela-Tgfa mice
Concomitant pancreatic activation of Kras(G12D) and Tgfa results in cystic papillary neoplasms reminiscent of human IPMN.
Age, Specimen part
View SamplesThe NfkB-pathway is activated early during acute pancreatitis. We investigated the influence on gene expression of two pancreas-specific deletions interfering with NfkB-activation. Pancreata from 8 week old mice were prepared, RNA was isolated and Affymetrix microarray expression analysis was performed.
Deletion of IkBa induces RelA to alleviate acute pancreatitis in mice through upregulation of Spi2a
Age, Specimen part, Disease, Disease stage, Time
View SamplesProfiling CD34+ BCR-ABL+ cells of CML patients in chronic phase or blast crisis to identify differentially expressed stage-specific genes.
Gene expression profiling of CD34+ cells identifies a molecular signature of chronic myeloid leukemia blast crisis.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesSynaptic dysfunction is thought to underlie altered sociability in autism. However, the gene regulatory mechanisms that control synaptic protein expression in the context of social behaviour are poorly explored. Here we show that deletion of the large placental mammal specific miR379-410 cluster in mice leads to hypersocial behaviour, increased excitatory synaptic transmission and exaggerated expression of ionotropic glutamate receptor complexes in the hippocampus. Thus, interfering with miR379-410 could represent a novel therapeutic strategy for social deficits in autism.
No associated publication
Sex, Age, Specimen part, Cell line
View SamplesAnalysis of newborn mouse epidermis lacking the expression of Insulin receptor (IR) and Insulin like growth factor 1 receptor (IGF-1R). Results show that IR/IGF-1R signalling control epidermal morphogenesis.
Insulin/IGF-1 controls epidermal morphogenesis via regulation of FoxO-mediated p63 inhibition.
No sample metadata fields
View SamplesBackground: Information on the carcinogenic potential of chemicals is only availably for High Production Volume products. There is however, a pressing need for alternative methods allowing for the chronic toxicity of substances, including carcinogenicity, to be detected earlier and more reliably. Here we applied advanced genomics to a cellular transformation assay to identify gene signatures useful for the prediction of risk for carcinogenicity. Methods: Genome wide gene expression analysis and qRT-PCR were applied to untransformed and transformed Balb/c 3T3 cells that exposed to 2, 4-diaminotoluene (DAT), benzo(a)pyrene (BaP), 2-Acetylaminoflourene (AAF) and 3-methycholanthrene (MCA) for 24h and 120h, at different concentrations, respectively. Furthermore, various bioinformatics tools were used to identify gene signatures predicting for the carcinogenic risk. Results: Bioinformatics analysis revealed distinct datasets for the individual chemicals tested while the number of significantly regulated genes increased with ascending treatment concentration of the cell cultures. Filtering of the data revealed a common gene signature that comprised of 13 genes whose regulation in cancer tissue has already been established. Strikingly, this gene signature was already identified prior to cell transformation therefore confirming the predictive power of this gene signature in identifying carcinogenic risks of chemicals. Comparison of fold changes determined by microarray analysis and qRT-PCR were in good agreement. Conclusion: Our data describes selective and commonly regulated carcinogenic pathways observed in an easy to use in vitro carcinogenicity assay. Here we defined a set of genes which can serve as a simply assay to predict the risk for carcinogenicity by use of an alternative in vitro testing strategy.
Toxicogenomics applied to in vitro carcinogenicity testing with Balb/c 3T3 cells revealed a gene signature predictive of chemical carcinogens.
Cell line, Treatment, Time
View SamplesWe recently reported isolation of various cancer progenitor cells of transgenic c-Myc and c-Raf mouse lung tumors [Reamon-Buettner SM and Borlak J, 2008]. As lung tumors can arise following dysregulation of signalling pathways normally activated during lung development we were particularly interested in investigating the genetic heterogeneity of these cancer cell lines. By whole genome expression analysis we identified two cell lines (A2C12, cRAF_cMYC) to be very different from the remaining tumor cells. Specifically the A2C12 and cRAF_cMYC cell lines expressed various stem cell markers, most notably CD34, CD44, Pdpn and Dlg7. Likewise, the A2C12 and cRAF_cMYC expressed the ATP-binding cassette (ABC) transporters Abcc1 and Abcg2 at different level when compared to other established cell lines. Furthermore, a genome wide expression profiling displayed differential gene expression pattern between and within progenitor cell lines. That provided important clues on heterogeneity in the signalling pathways amongst the cancer cell lines. We also knock down CD44 using a retroviral delivery system and observed an increased G1 peak and apoptosis as determined by flow cytometry. Finally, we analyzed promoters of regulated genes and identified overrepresented 18 transcription factor binding sites (TFBS) in common regulated genes, 10 unique TFBS in A2C12 and 9 unique TFBS in cRaf_cMyc. These data indicates that our tumor cell lines are suitable models to study the biology of lung cancer progenitor cell. Most importantly, we show that our tumor cell lines do not represent a homogeneous population of tumor-initiating cells. Understanding heterogeneity in tumors will lead to new diagnostic and therapeutic approaches.
No associated publication
Disease, Disease stage, Cell line
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