We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C- isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling.
Insulin decreases atherosclerosis by inducing endothelin receptor B expression.
Age, Specimen part, Disease, Disease stage, Treatment
View Samples10 day old seedlings were treated with 5uM of the cytokinin Benzyladenine(BA)or DMSO at 15min, 45min, 120min, 480min and 1440min
Expression profiling of cytokinin action in Arabidopsis.
Age, Compound, Time
View SamplesThese E. coli strains were grown with various signaling molecules and the expression profiles were determined.
Global effects of the cell-to-cell signaling molecules autoinducer-2, autoinducer-3, and epinephrine in a luxS mutant of enterohemorrhagic Escherichia coli.
No sample metadata fields
View SamplesEnterohemorrhagic E. coli (EHEC) colonizes the large intestine and causes attaching and effacing lesions (AE). Most of the genes involved in the formation of AE lesions are encoded within a chromosomal pathogenicity island termed the Locus of Enterocyte Effacement (LEE). The LysR-like transcriptional factor QseA regulates the LEE by binding directly to the regulatory region of ler. Here, we performed transcriptome analyses comparing WT EHEC and the isogenic qseA mutant in order to elucidate the extent of QseAs role in gene regulation in EHEC. The following results compare genes that were up-regulated and down-regulated ! 2-fold in the qseA mutant strain compared to the WT strain. At mid-exponential growth, 222 genes were up-regulated and 1874 were downregulated. At late-exponential growth, a total of 55 genes were up-regulated and 605 genes were down-regulated. During mid-exponential growth, QseA represses its own transcription, whereas during late-logarithmic growth, QseA activates expression of the LEE genes as well as non-LEE encoded effector proteins. During both growth phases, several genes carried in O-islands, were activated by QseA, whereas genes involved in cell metabolism were repressed. We also performed electrophoretic mobility shift assays, competition experiments, and DNAseI footprints, and the results suggested that QseA directly binds both the ler proximal and distal promoters, its own promoter, as well as promoters of genes encoded in EHEC-specific O-islands. Additionally, we mapped the transcriptional start site of qseA, leading to the identification of two promoter sequences. Taken together, these results indicate that QseA acts as a global regulator in EHEC, coordinating expression of virulence genes.
The LysR-type regulator QseA regulates both characterized and putative virulence genes in enterohaemorrhagic Escherichia coli O157:H7.
No sample metadata fields
View SamplesTransgenerational effects of parental metabolic state have been shown, but the mechanism is still unclear. Here we present transcriptome sequencing data from AKHR heterozygous F1 progeny, either from obese maternal or paternal parents, compared to genetically matched heterozygous controls or to wild-type controls Overall design: 3 AKHR heterozygous samples descended from obese maternal parents, 3 AKHR heterozygous samples descended from obese paternal parents, 3 AKHR heterozygous samples descended from non-obese parents, and 3 wild-type controls, independent biological replicates and independent experimental replicates (1 set of samples from each experimental replicate)
Parental obesity leads to metabolic changes in the F2 generation in <i>Drosophila</i>.
Specimen part, Subject
View SamplesRegulatory T cells (Treg cells) expressing the forkhead family transcription factor Foxp3 are critical mediators of dominant immune tolerance to self. Most Treg cells constitutively express the high-affinity interleukin 2 (IL-2) receptor alpha-chain (CD25); however, the precise function of IL-2 in Treg cell biology has remained controversial. To directly assess the effect of IL-2 signaling on Treg cell development and function, we analyzed mice containing the Foxp3gfp knock-in allele that were genetically deficient in either IL-2 (Il2-/-) or CD25 (Il2ra-/-). We found that IL-2 signaling was dispensable for the induction of Foxp3 expression in thymocytes from these mice, which indicated that IL-2 signaling does not have a nonredundant function in the development of Treg cells. Unexpectedly, Il2-/- and Il2ra-/- Treg cells were fully able to suppress T cell proliferation in vitro. In contrast, Foxp3 was not expressed in thymocytes or peripheral T cells from Il2rg-/- mice. Gene expression analysis showed that IL-2 signaling was required for maintenance of the expression of genes involved in the regulation of cell growth and metabolism. Thus, IL-2 signaling seems to be critically required for maintaining the homeostasis and competitive fitness of Treg cells in vivo.
A function for interleukin 2 in Foxp3-expressing regulatory T cells.
No sample metadata fields
View SamplesEscherichia coli 8624 and the isogenic mutants in qseE, qseF and qseG are compared to determine the role that each of the genes play in regulation of the transcriptome. These results are verified by qRT-PCR and reveal the important role of this three-component signaling system.
The two-component system QseEF and the membrane protein QseG link adrenergic and stress sensing to bacterial pathogenesis.
No sample metadata fields
View SamplesWe investigated an acute kidney injury (AKI) model in rats induced by cisplatin (Cp) administration. The cisplatin is widely used since its biochemical and histopathological characteristics are representative of drug-induced AKI in humans. Male Wistar rats were dosed once ip with 0, 1 and 3 mg/kg cisplatin. Tubular necorsis was observed histopathologically in all treated rats and war recovery on day 26. Gene expression profiling of the kidney cortex with microarrays 3, 5, 8, and 26 days after single administration of 3mg/kg Cp revealed a major profile pattern characterized by maximally increased and decreased mRNA levels on day 8, with clear changes already found 3 days after treatment for about half of the mRNAs. The mRNA expression pattern after administration of 1mg/kg Cp was overall similar, yet with a dose-dependent smaller fold-change. In summary we found 274 mRNAs showing significantly altered levels in the kidney of which 162 were increased and 112 decreased, respectively. Functional interpretation of the proteins encoded by these mRNAs revealed induction of a DNA damage response likely caused by the known molecular activity of Cp as DNA alkylating agent. Increased mRNAs associated with apoptosis (encoded by the corresponding genes like B-cell lymphoma 3-encoded protein, Bcl3; mouse double minute 2 homolog, Mdm2; p21/WAF1 also known as cyclin-dependent kinase inhibitor 1), cell cycle regulation (encoded by the corresponding genes like Cyclin-G1, Ccng1; B-cell translocation gene 2, Btg2) and stress response may have partly been induced by the DNA damage, but also by the kidney damage associated with Cp administration. Increased levels of mRNAs indicating regeneration (encoded by the corresponding genes like SPARC- related modular calcium-binding protein 2, Smoc2; Tenascin C, Tnc) and decreased levels of mRNAs coding for proteins related to kidney function, indicating dedifferentiation, are likely related to the observed kidney injury.
Comparison of the MesoScale Discovery and Luminex multiplex platforms for measurement of urinary biomarkers in a cisplatin rat kidney injury model.
Sex, Specimen part
View SamplesWe used microarrays to assess gene expression changes in cells with siRNA-mediated knockdown of OPG compared to normal cells. Furthermore, we used microarrays to assess gene expression in cells treated with either RANKL or TRAIL compared to vehicle-treated cells.
No influence of OPG and its ligands, RANKL and TRAIL, on proliferation and regulation of the calcification process in primary human vascular smooth muscle cells.
Specimen part, Treatment
View SamplesWe used the microarrays to obtain the cancerous signatures of T-cell, B-cell, erythroid and megakaryoblastic leukemias in mice.
Gene profiling of the erythro- and megakaryoblastic leukaemias induced by the Graffi murine retrovirus.
No sample metadata fields
View Samples