The goals of the microarray experiment were to determine the role of MAF1, the Toxoplasma gondii mediator of host mitochondrial association, on host cell gene expression by comparing infection of WT cells with Type II and Type II:MAF1 parasites. We also explored the role of MAF1 on host cell gene expression by comparing profiles of WT and MAVS KO MEFs infected with Type I and Type Imaf1KO parasites.
Toxoplasma effector MAF1 mediates recruitment of host mitochondria and impacts the host response.
Specimen part, Time
View SamplesE-cadherin (E-cad) mediates cell-cell adhesion and has been proposed to suppress both invasion and metastasis. However, invasive ductal cancers retain E-cad expression in the primary tumor, circulating tumor cells, and distant metastases. We recently demonstrated that cancer cell clusters are efficient metastatic seeds. Since clusters organize through cell-cell adhesion, we tested the requirement for E-cad in genetically engineered mouse models of luminal and basal breast cancer. Loss of E-cad increased invasion and dissemination in 3D culture and in the mammary gland. However, E-cad loss also reduced cancer cell proliferation, survival, tumor cell seeding, and metastatic outgrowth in the lungs. At the transcript level, loss of E-cad was associated with increased apoptosis. Consistent with these results, inhibition of apoptosis partially rescued the metastatic phenotype of E-cad null cancer cells. We therefore propose that E-cad is an invasion suppressor, survival factor, and metastasis promoter in invasive ductal cancers. Overall design: Differential gene expression analysis between organoids isolated from adeno-Cre transduced MMTV-PyMT E-cad+/+ (r = 4 biological replicates) and adeno-Cre transduced MMTV-PyMT E-cadfl/fl (r = 5 biological replicates)
E-cadherin is required for metastasis in multiple models of breast cancer.
Specimen part, Cell line, Treatment, Subject
View SamplesComplete transcriptome profiling in human failing and non-failing control hearts using next-gen sequencing Overall design: Poly-A selected RNA and small RNA sequencing carried out in 5 groups of samples: NF, ICM, NICM, ICM+LVAD, NICM+LVAD
Deep RNA sequencing reveals dynamic regulation of myocardial noncoding RNAs in failing human heart and remodeling with mechanical circulatory support.
Specimen part, Disease, Subject
View SamplesPurpose: provide evidence that RNA-seq can add information to transcriptome profiling already discovered by other technologies for atopic dermatitis Methods: mRNA profiles of 20 atopic dermatitis were analyzed to compare lesional and non-lesional skin, then transcriptomes found by reads were compared to Microarray and RT-PCR Results:RNA-seq provided complementary genes to AD transcriptome IL-36 and TREM-1 Conclusions: Our study represents the first analysis of lesional AD tissue by RNA-seq and comparison to microarray and RT-PCR Overall design: paired biopsies from lesional and non-lesional tissue of 20 patients sequenced by RNA-seq
RNA sequencing atopic dermatitis transcriptome profiling provides insights into novel disease mechanisms with potential therapeutic implications.
No sample metadata fields
View SamplesIn this study we applied genomic profiling to evaluate the transcriptomic differences between murine models ot atopic dermatitis.
Major differences between human atopic dermatitis and murine models, as determined by using global transcriptomic profiling.
Sex, Specimen part, Treatment
View SamplesMurine gliomblastoma tumor progenitor cells TPCs with high and low EGFRvIII activity, pEGFR-Hi and pEGFR-Lo, showed differences in proliferation, differentiation, and invasion. Zs-Green-expressing
GBM heterogeneity as a function of variable epidermal growth factor receptor variant III activity.
Specimen part
View SamplesA major impediment to the effective treatment of patients with PDAC (Pancreatic Ductal Adenocarcinoma) is the molecular heterogeneity of the disease, which is reflected in an equally diverse pattern of clinical responses to therapy. We developed an efficient strategy in which PDAC samples from 17 consecutively patients were obtained by EUS-FNA or surgery, their cells maintained as a primary culture and tumors as breathing tumors by xenografting in immunosuppressed mice. For these patients a clinical follow up was obtained. On the breathing tumors we studied the RNA expression profile by an Affymetrix approach. We observed a significant heterogeneity in their RNA expression profile, however, the transcriptome was able to discriminate patients with long- or short-time survival which correspond to moderately- or poorly-differentiated PDAC tumors respectively. Cells allowed us the possibility to analyze their relative sensitivity to several anticancer drugs in vitro by developing a chimiogram, like an antibiogram for microorganisms, with several anticancer drugs for obtaining an individual profile of drug sensitivity and as expected, the response was patient-dependent. Interestingly, using this approach, we also found that the transcriptome analysis could predict the sensitivity to some anticancer drugs of patients with a PDAC. In conclusion, using this approach, we found that the transcriptome analysis could predict the sensitivity to some anticancer drugs and the clinical outcome of patients with a PDAC.
Transcriptomic analysis predicts survival and sensitivity to anticancer drugs of patients with a pancreatic adenocarcinoma.
Sex, Age, Specimen part
View SamplesWe undertook an inter-laboratory effort to generate high-quality quantitative data for a very large number of cellular components in yeast using transcriptome and metabolome analysis. We ensured the high-quality of the experimental data by evaluating a wide range of sampling and measurement techniques. The data were generated for two different yeast strains, each growing under two different growth conditions and based on integrated analysis of the high-throughput data we hypothesize that differences in growth rates and yields on glucose between the two strains are due to differences in protein metabolism.
Integrated multilaboratory systems biology reveals differences in protein metabolism between two reference yeast strains.
No sample metadata fields
View SamplesThe synthetic supercooling drug, icilin, and its primary receptor target, the cation channel transient receptor potential (TRP) melastatin-8 (TRPM8), have been described as potent negative regulators of inflammation in the colon. The aim of this study was to determine whether the anti-inflammatory action of icilin could potentially be used to treat autoimmune neuroinflammatory disorders, such as multiple sclerosis (MS). During experimental autoimmune encephalomyelitis (EAE)a CD4+ T celldriven murine model of MSwe found that both wild-type (WT) and TRPM8-deficient EAE mice were protected from disease progression during icilin treatment, as evidenced by delays in clinical onset and reductions in neuroinflammation. In vitro, icilin potently inhibited the proliferation of murine and human CD4+ T cells, with the peripheral expansion of autoantigen-restricted T cells similarly diminished by the administration of icilin in mice. Attenuation of both TRPM8-/- and TRP ankyrin-1-/- T cell proliferation by icilin was consistent with the WT phenotype, which suggests a mechanism that is independent of these channels. In addition, icilin treatment altered the expressional profile of activated CD4+ T cells to one that was indicative of restricted effector function and limited neuroinflammatory potential. These findings identify a potent anti-inflammatory role for icilin in lymphocyte-mediated neuroinflammation and highlight clear pleiotropic effects of the compound beyond classic TRP channel activation.
The cooling compound icilin attenuates autoimmune neuroinflammation through modulation of the T-cell response.
Sex, Specimen part
View SamplesAnalysis of undifferentiated pleomorphic sarcoma/malignant fibrous histiocytoma-like tumors from LSL-KrasG12D, p53Fl/Fl mouse model of soft tissue sarcoma.
Cross species genomic analysis identifies a mouse model as undifferentiated pleomorphic sarcoma/malignant fibrous histiocytoma.
Specimen part
View Samples