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SRP043192
Escherichia coli
4 Downloadable Samples
Illumina HiSeq 2000
Description
Exponentially growing cells and type II persister cells from the DS1-(hipQ)-strain
Publication Title
Novel protocol for persister cells isolation.
Sample Metadata Fields
Specimen part, Disease, Cell line
View Samples- Homo sapiens
- 18 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
The main objective of this study is to identify the list of genes differentially expressed between infected with Leishmania braziliensis and non-infected macrophage cultures based on gene expression microarray profiling
Publication Title
Changes in Macrophage Gene Expression Associated with Leishmania (Viannia) braziliensis Infection.
Sample Metadata Fields
Specimen part
View Samples- Drosophila melanogaster
- 48 Downloadable Samples
- NextSeq 500
Description
A-to-I RNA editing levels differ across tissues and cell types, but regulators of the editing process are largely unknown. We used RNA-seq on whole fly brains with different RNA binding proteins knocked down to test for A-to-I RNA editing level differences between controls and knockdowns. Overall design: To screen for editing regulators in the Drosophila brain, we crossed a pan-neuronal Gal4 driver, C155-Gal4, to different UAS-shRNA lines targeting individual RNA binding proteins, extracted RNA and made RNA-seq libraries. We sequenced four total replicates of shGFP controls and two replicates of all RNA binding protein knockdowns.
Publication Title
Zinc Finger RNA-Binding Protein Zn72D Regulates ADAR-Mediated RNA Editing in Neurons.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Mus musculus
- 34 Downloadable Samples
- Illumina HiSeq 2500
Description
Microglia are the resident myeloid-lineage cells in the central nervous system. Despite myriad observations of microglia associated with various tissue pathologies in degenerative disease, their function in and contributions to the pathophysiological processes remain unclear. It is particularly uncertain whether microglia act harmfully to contribute to worsening of degeneration, act beneficially to combat disease-related dysfunction, or perform functions that result in both outcomes. In this dataset, we report RNA sequencing results from mice that undergo inducible ALS/FTLD-like degeneration and subsequent recovery. The goals were to identify whether microglia show transcriptional signatures commensurate with the disease stage or if they remain constant throughout. Additionally, we sought to understand whether there was a particular transcriptional or functional signature associated with functional recovery in the mice. The latter could lead to an understanding of how microglia may be targeted to combat disease and enhance recovery following or during degeneration. Overall design: mRNA profiles from microglia sorted from whole-spinal cord taken from doxycycline (DOX) inducible NEFH-tTa/tetO-208-hTDP43 (rNLS8, (+/+)) mice. In these mice, removal of doxycycline from the diet (DOX-OFF) induces transgenic expression and degeneration and reintroduction (DOX-ON) suppresses expression and enables recovery. We report profiles from rNLS8 mice that were DOX-OFF for 2 weeks (N=8) or 6 weeks (N=7), or DOX-OFF for 6 weeks followed by DOX-ON for 1 week (N=9). We also report profiles from control samples that include: rNLS8 mice that were DOX-ON for 6 weeks (N = 6) as asymptomatic genetic controls and WT (-/-) littermates that were DOX-OFF for 2 weeks (N=4), 6 weeks (N=1), or DOX-OFF for 6 weeks followed by 1 week DOX-ON (N=3) as asymptomatic doxycycline controls.
Publication Title
Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A novel crosstalk between CCAR2 and AKT pathway in the regulation of cancer cell proliferation.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
CCAR2 is a nuclear protein recently emerged as a pivotal player of the DNA damage response since it has been found involved in both apoptosis induction and DNA repair. Differently, its role in tumorigenesis and cancer progression is still elusive. In our studies we found that CCAR2 depletion impairs the proliferation of human cancer cell lines, but leaves unaffected the growth of normal immortalized cells. To better investigate this point we performed a genome wide gene expression analyses in U2OS and BJ-hTERT depleted of CCAR2 and we found that loss of this protein causes the deregulation of genes implicated in the AKT pathway specifically in U2OS cells, but not in BJ-hTERT. In accordance with these results we found a reduction in AKT activation in all the tested cancer cell lines depleted of CCAR2, but not in the normal ones. The defective activation of AKT is caused by the upregulation of TRB3 gene in cancer cells depleted of CCAR2 and finally results in the reduction of GSK3 phosphorylation, prevention of G1/S transition and inhibition of cancer cell growth.
Publication Title
A novel crosstalk between CCAR2 and AKT pathway in the regulation of cancer cell proliferation.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
CCAR2 is a nuclear protein recently emerged as a pivotal player of the DNA damage response since it has been found involved in both apoptosis induction and DNA repair. Differently, its role in tumorigenesis and cancer progression is still elusive. In our studies we found that CCAR2 depletion impairs the proliferation of human cancer cell lines, but leaves unaffected the growth of normal immortalized cells. To better investigate this point we performed a genome wide gene expression analyses in U2OS and BJ-hTERT depleted of CCAR2 and we found that loss of this protein causes the deregulation of genes implicated in the AKT pathway specifically in U2OS cells, but not in BJ-hTERT. In accordance with these results we found a reduction in AKT activation in all the tested cancer cell lines depleted of CCAR2, but not in the normal ones. The defective activation of AKT is caused by the upregulation of TRB3 gene in cancer cells depleted of CCAR2 and finally results in the reduction of GSK3 phosphorylation, prevention of G1/S transition and inhibition of cancer cell growth.
Publication Title
A novel crosstalk between CCAR2 and AKT pathway in the regulation of cancer cell proliferation.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Vaccination reduces morbidity and mortality from pneumonia but its effect on the tissue-level response to infection is still poorly understood. We evaluated pneumonia disease progression, acute phase response and lung gene expression profiles in mice inoculated intranasally with virulent gram-positive Streptococcus pneumoniae serotype (ST) 3, with and without prior immunization with pneumococcal polysaccharide ST 3 (PPS3), or co-immunization with PPS3 and with a low dose of lipopolysaccharide (LPS). Pneumonia severity was assessed in the acute phase, 5, 12, 24 and 48 h post-inoculation (p.i.) and the resolution phase of 7 days p.i. Primary PPS3 specific antibody production was upregulated and IgM binding to pneumococci increased in PPS3-immunized mice. Immunizations with PPS3 or PPS3 + LPS decreased bacterial recovery the lung and blood at 24 and 48 h and increased survival. Microarray analysis of whole lung RNA revealed significant changes in the acute phase protein serum amyloid A (SAA) between noninfected and infected mice, which were attenuated by immunization. SAA transcripts were higher in the liver and lungs of infected controls, and SAA protein was elevated in serum, but decreased in PPS3-immunized mice. Thus, during a virulent pneumonia infection, prior immunization with PPS3 in an IgM-dependent manner as well as co-immunization with PPS3 + LPS attenuated pneumonia severity and promoted resolution of infection, concomitant with significant regulation of cytokine gene expression in the lungs, and acute phase proteins in the lungs, liver and serum.
Publication Title
Immunization with pneumococcal polysaccharide serotype 3 and lipopolysaccharide modulates lung and liver inflammation during a virulent Streptococcus pneumoniae infection in mice.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
Numerous pathways underlie brain invasion by tumors, a critical element underpinning recurrence and lethality in human glioblastomas (hGBMs). The identification of the master factors that elicit these pathways globally, driving invasion altogether, eludes us. We report that high expression levels of non-canonical Wnt5a characterize the most invasive gliomas, epitomize dismal prognosis and discriminate the most infiltrating mesenchymal hGBMs from proneural and classical ones. Exacerbated Wnt5a defines mesenchymal hGBM cells (Wnt5aHigh) possessing prototypical invasiveness and tumor-promoting stem-like characteristics (TPCs), but not their Wnt5aLow siblings. While inhibition of Wnt5a suppresses infiltration in mesenchymal hGBM TPCs, administration or over-expression of Wnt5a elicits the opposite effects, turning on infiltrative mesenchymal-like molecular programs in poorly motile, classical hGBM TPCs and Wnt5aLow mesenchymal TPCs, ex vivo and intracranially. Anti-Wnt5a antibodies or antagonist Wnt5a peptides block invasion, increasing survival in clinically relevant intracranial hGBM models. Wnt5a emerges as a master regulator in gliomatous invasion, endowing hGBM TPCs with archetypal, infiltratory transcriptional and functional profiles, providing a unique target to tackle brain invasion by hGBM cancer stem cells.
Publication Title
Wnt5a Drives an Invasive Phenotype in Human Glioblastoma Stem-like Cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Analysis of genes regulated by STC1 down-regulation in mouse 4T1 derived clone, 4T1ch9. STC1 expression is associated with tumor growth and metastasis. This study looks at genes affected when STC1 expression is down-regulated by STC1 shRNA.
Publication Title
STC1 expression is associated with tumor growth and metastasis in breast cancer.
Sample Metadata Fields
Cell line
View Samples