miR-34a and miR-34b/c genes are frequently epigenetically silenced in primary CRCs. However, the in vivo relevance of miR-34a/b/c for suppression of intestinal tumor formation has not been analyzed by genetic approaches. ApcMin/+ mice with deletion of the miR-34a and miR-34b/c genes were generated and analyzed. The mRNA expression profiles of intestinal adenomas with and without functional miR-34a/b/c genes were compared. Overall design: miR-34a/b/c deficient ApcMin/+ mice and wild-type ApcMin/+ mice were sacrificed at 18 weeks of age. 3 tumor RNA samples were obtained for each genotype; each tumor RNA sample represented a pool of 3 tumors isolated from the same mouse.
<i>miR-34a</i> and <i>miR-34b/c</i> Suppress Intestinal Tumorigenesis.
Age, Cell line, Subject
View SamplesWe employ mRNA-seq to investigate transcriptome of Pum1-Knockout, Pum2-Knockout and WT conditons Overall design: In order to investigate whether Pum1 and Pum2 regulate their targets at their RNA levels, we used 1/10 of the samples from the Pum1 and Pum2 iCLIP experiments (four biological repeats of WT, P1KO, and P2KO neonatal brains) to extract total RNAs for RNA deep sequencing. And we also collected three Ndcko neonatal brains for RNA deep sequencing.
Post-transcriptional regulation of mouse neurogenesis by Pumilio proteins.
Subject
View SamplesGene expression analysis performed on FACS sort purified GC LZ and DZ cells of either high or low affinity to identify unique gene signatures.
Differentiation of germinal center B cells into plasma cells is initiated by high-affinity antigen and completed by Tfh cells.
Sex, Specimen part
View SamplesGene expression analysis performed on FACS sort purified GC LZ and DZ cells of either high and low affinity to identify unique gene signatures.
Differentiation of germinal center B cells into plasma cells is initiated by high-affinity antigen and completed by Tfh cells.
Sex, Specimen part
View SamplesActivity-dependent gene expression is central for sculpting neuronal connectivity in the brain. Despite the importance for synaptic plasticity, a comprehensive analysis of the temporal changes in the transcriptomic response to neuronal activity is lacking. In a genome wide survey we identified genes that were induced at 1, 4, 8, or 24 hours following neuronal activity in the hippocampus.
Genome-wide profiling of the activity-dependent hippocampal transcriptome.
Sex, Age, Specimen part, Time
View SamplesDNA microarrays were used to investigate global gene expression patterns in cultured human umbilical vein endothelial cells (HUVEC) exposed to 1 nmol/L estradiol for 24 hours, compared to control cells.
Estradiol stimulates vasodilatory and metabolic pathways in cultured human endothelial cells.
Specimen part, Time
View SamplesThe gut microbiota has been implicated in obesity and cardiometabolic diseases, although evidence in humans is scarce. We investigated how gut microbiota manipulation by antibiotics (7-day administration of amoxicillin, vancomycin, or placebo) affects host metabolism in 57 obese, prediabetic men. Vancomycin, but not amoxicillin, decreased bacterial diversity and reduced Firmicutes involved in short-chain fatty acid and bile acid metabolism, concomitant with altered plasma and/or fecal metabolite concentrations. Adipose tissue gene expression of oxidative pathways was upregulated by antibiotics, whereas immune-related pathways were downregulated by vancomycin. Antibiotics did not affect tissue-specific insulin sensitivity, energy/substrate metabolism, postprandial hormones and metabolites, systemic inflammation, gut permeability, and adipocyte size. Importantly, energy harvest, adipocyte size, and whole-body insulin sensitivity were not altered at 8-week follow-up, despite a still considerably altered microbial composition, indicating that interference with adult microbiota by 7-day antibiotic treatment has no clinically relevant impact on metabolic health in obese humans.
Effects of Gut Microbiota Manipulation by Antibiotics on Host Metabolism in Obese Humans: A Randomized Double-Blind Placebo-Controlled Trial.
Sex, Specimen part, Disease, Disease stage, Treatment, Subject, Time
View SamplesAging and neurodegeneration are often accompanied by a functionally impaired ubiquitin-proteasome system (UPS). In tauopathies and polyglutamine diseases a mutant form of Ubiquitin B, UBB+1, accumulates in disease-specific aggregates. UBB+1 mRNA is generated at low levels in vivo during transcription from the Ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB+1 accumulation, we used a UBB+1 expressing transgenic mouse line, that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimers disease (AD). In order to reveal affected organs and functions, young and aged UBB+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wildtype littermate mice. Accordingly, UBB+1 was strongly expressed in brainstem regions of transgenic mice controlling respiration. These regions included, for example, the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nuclei. In addition, UBB+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented controls. We conclude that long-term UPS inhibition due to UBB+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients.
Long-term proteasomal inhibition in transgenic mice by UBB(+1) expression results in dysfunction of central respiration control reminiscent of brainstem neuropathology in Alzheimer patients.
No sample metadata fields
View SamplesTo characterize the transcriptome of the transcription factor AP4 DLD-1 cells were infected with AP4 coding viruses for different periods of time. Adenovirus amplification and purification was performed as previously described (He et al., 1998). The minimal amount of virus needed to reach more than 90% infection efficiency was determined by monitoring GFP signals with fluorescence microscopy. DLD-1 cells were infected in serum-free medium with adenovirus for 3 hours. After removal an equal amount of medium containing 20% FBS was added.
AP4 is a mediator of epithelial-mesenchymal transition and metastasis in colorectal cancer.
Cell line, Time
View SamplesIn order to comprehensively identify RNA-expression changes after p53-activation, total RNA was isolated and subjected to next generation seqencing (RNA-Seq) after activation of a conditional p53 allele in SW480 cells. Overall design: SW480/pRTR-p53-VSV cells were subjected to RNA-Seq analysis after 48 hours doxycycline-treatment.
p53-Regulated Networks of Protein, mRNA, miRNA, and lncRNA Expression Revealed by Integrated Pulsed Stable Isotope Labeling With Amino Acids in Cell Culture (pSILAC) and Next Generation Sequencing (NGS) Analyses.
No sample metadata fields
View Samples