Th17 cells are believed to be a critical cell population for driving autoimmune diseases. However, environmental factors that are directly related to the development of Th17 cells are largely unknown.
Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells.
Specimen part
View SamplesOct3/4, Sox2, Klf4, and c-Myc re-wire somatic cells to achieve induced pluripotency (iPS cells). However, subtle differences in reprogramming methodology may confound comparative studies of reprogramming-induced gene expression changes. We specifically focused on the design of polycistronic reprogramming constructs, which encode all four factors linked with 2A peptides. Notably, publically available cassettes were found to employ one of two Klf4 variants (Klf4S and Klf4L; GenBank Accession Nos: AAC52939.1 and AAC04892.1), differing only by nine N-terminal amino acids. In a polycistronic context, these two variants generated dissimilar protein stoichiometry, where Klf4L vectors produced more Klf4 protein than those encoding Klf4S.
KLF4 N-terminal variance modulates induced reprogramming to pluripotency.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Induced pluripotent mesenchymal stromal cell clones retain donor-derived differences in DNA methylation profiles.
Specimen part, Subject
View SamplesReprogramming of somatic cells into induced pluripotent stem cells (iPSC) is an epigenetic phenomenon. We have reprogrammed mesenchymal stromal cells (MSC) from human bone marrow by retrovirus-mediated overexpression of OCT-3/4, SOX2, c-MYC, and KLF4. This series summarizes gene expression profiles of eight iP-MSC clones derived from three different donors. These datasets were subsequently used for PluriTest analysis (Muller FJ, Schuldt B et al., Nat. Methods 2011; 8: 315-317) demonstrating that all iP-MSC clones were clearly associated with pluripotent cells.
Induced pluripotent mesenchymal stromal cell clones retain donor-derived differences in DNA methylation profiles.
Specimen part
View SamplesMicroarrays were used to examine the genome-wide expression in FIH null, VHL null and VHL/FIH double null MEFs.
The asparaginyl hydroxylase factor inhibiting HIF-1alpha is an essential regulator of metabolism.
Specimen part
View SamplesEffects of treatment with Nimodipine on N9 cells
Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis.
Treatment
View SamplesIn mouse bone marrow, mesenchymal stem cells (MSC) has the potential to form osteocytes, adipocytes and cartilage. In the process of osteogenesis, MSCs differenetiate into stromal cells, such as CAR cells. Osteoblast is responsible for the formation of osteocytes and osteoblasts may be differentiated from a subset of CAR cells. Dmp1-Cre targeted CAR cells are thought to enrich for a osteoblast progenitor population.
Targeting of Mesenchymal Stromal Cells by Cre-Recombinase Transgenes Commonly Used to Target Osteoblast Lineage Cells.
Age, Specimen part
View SamplesMicroarray analysis was performed to examine potential differences in target gene expression of AE9a expressing low cells compared to AE9a expressing high cells. Potential contributing factors to AE9a induced leukemia were investigated.
Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation.
Specimen part
View SamplesThe experiment aims to identify mRNAs regulated in response to RelA
Role of CCL20 mediated immune cell recruitment in NF-κB mediated TRAIL resistance of pancreatic cancer.
Specimen part, Treatment
View SamplesRetinal cells are specified in a zebrafish recessive mutant called young (yng) but they fail to terminally differentiate; i.e. extend neurites and make synaptic contacts. A point mutation in a brahma-related gene 1 (brg1) is responsible for this phenotype. In this microarray study, a three-factor factorial design was utilized to investigate the effects of 1) mutation, 2) change in time (36 vs. 52hpf), and 3) change in tissue (retina vs. whole embryos), and their interactions on gene expression. Significant probesets were inferred by using both specific contrasts of the fitted Analysis of Variance (ANOVA) models and a corresponding 2-fold expression cutoff. The probesets were grouped into three broad categories: 1) Brg1-regulated retinal differentiation genes (731 probsets), 2) Retinal specific genes but independent of Brg1 regulation (3038 probesets) and 3) Genes regulated by Brg1 but outside the retina (107 probesets). Four gene groups/pathways including neurite outgrowth regulators, Delta-Notch signalling molecules, Irx family members and specific cell cycle regulators were identified in the first group, and their relevance for retinal differentiation functionally validated. This study demonstrates that an approach such as ours can identify relevant genes and pathways involved in retinal development as well as the development of other tissues at the same time.
Factorial microarray analysis of zebrafish retinal development.
Specimen part
View Samples