The emergence of multidrug resistant (MDR) Mycobacterium tuberculosis (Mtb) strains, resistant to the frontline anti-tubercular drugs rifampicin and isoniazid, forces treatment with less effective and toxic second-line drugs and stands to derail TB control efforts. However, the immune response to MDR Mtb infection remains poorly understood. Here, we determined the RNA transcriptional profile of in vitro generated macrophages to infection with either drug susceptible Mtb HN878 or MDR Mtb W_7642 infection. Overall design: Bone marrow-derived macrophages (BMDMs) from WT and Il1r1–/– mice were derived in 7 days in GM-CSF supplemented complete DMEM. Cells were infected with either Mtb HN878 or Mtb W_7642 (multiplicity of infection = 1) and RNA samples collected after 6 days.
Mycobacterium tuberculosis carrying a rifampicin drug resistance mutation reprograms macrophage metabolism through cell wall lipid changes.
Cell line, Subject
View SamplesSeedlings of 35 different Arabidopsis thaliana ecotypes were compared. Triplicates were performed of 10 ecotpyes, single arrays of 25 ecotypes.
Diversity of flowering responses in wild Arabidopsis thaliana strains.
Specimen part
View SamplesMultiple Sclerosis (MS) is an immune-mediated chronic inflammatory disease affecting the central nervous system. The cause of MS is not known and the mechanism of IFN-beta, a disease-modifying treatment (DMT) approved for MS, is not well-understood. Oligonucleotide microarrays were used to study gene expression in plasmacytoid denditic cells (pDCs) which are antigen-presenting cells implicated in MS pathogenesis.
Multiple sclerosis-linked and interferon-beta-regulated gene expression in plasmacytoid dendritic cells.
Sex, Age, Specimen part, Disease, Disease stage, Subject
View SamplesTranscripts (mRNA) during amino acid limitation after MEK was inhibited were analyzed.
A mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK)-dependent transcriptional program controls activation of the early growth response 1 (EGR1) gene during amino acid limitation.
Cell line, Treatment
View SamplesThe transcriptional regulator AmpR controls expression of the AmpC -lactamase in P. aeruginosa and other bacteria. Studies have demonstrated that in addition to regulating ampC expression, AmpR also regulates the expression of the sigma factor AlgT/U and the production of some quorum-sensing regulated virulence factors. In order to understand the ampR regulon, we compared the expression profiles of PAO1 and its isogenic ampR mutant, PAOampR in the presence and absence of sub-MIC -lactam stress. The analysis demonstrates that the ampR regulon is much more extensive than previously thought, with the deletion of ampR affecting the expression of over 300 genes. Expression of an additional 207 genes are affected by AmpR when the cells are exposed to sub-MIC -lactam stress, indicating that the ampR regulon in P. aeruginosa is much more extensive than previously thought.
The regulatory repertoire of Pseudomonas aeruginosa AmpC ß-lactamase regulator AmpR includes virulence genes.
Specimen part
View SamplesWe used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with paclitaxel, to aide in identifing the mechnism of action of elesclomol.
Elesclomol induces cancer cell apoptosis through oxidative stress.
No sample metadata fields
View SamplesWe used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with NAC, to aide in identifing the mechnism of action of elesclomol.
Elesclomol induces cancer cell apoptosis through oxidative stress.
No sample metadata fields
View SamplesCells can survive effector caspase (caspase 3/7) activation in response to transient apoptotic stimuli, a process named anastasis. To characterize the molecular events that occur during anastasis, we performed whole transcriptome RNA sequencing of untreated, apoptotic, and recovering cells. We found that anastasis is an active, two-stage program with unique transcriptional profiles in each stage. We also identified 10 genes that specific to the early stage of anastasis. Overall design: 3hr ethanol treatment was used to induce apoptosis in Hela cells. Ethanol was washed away after 3hr treatment to allow cells to recover. Total RNA was prepared from mock-treated cells, ethanol-treated cells and cells after 1hr, 2hr, 3hr, 4hr, 8hr, 12hr recovery, followed by ribosomal RNA depletion. 3 biological replicates were included for each group. Sequencing was done using Ion Proton.
A molecular signature for anastasis, recovery from the brink of apoptotic cell death.
Cell line, Treatment, Subject
View SamplesIn murine models, we find that irradiation of Paneth cells caused a gain of a stem cell-like transcriptome and induced activation of the Notch signaling pathway. This study documents plasticity by Paneth cells, a fully committed cell population to participate in epithelial replenishment following stem cell loss. Overall design: Single-cell dissociation was carried out as previously described (Li et al., 2016; Sato et al., 2011). Cell pellets were washed with cold PBS and re-suspended in FACS buffer. Cells were stained with DAPI, PerCP/Cy5.5-conjugated EpCAM, BUV395-conjugated CD45, and APC/fire 750-conjugated CD24. Cell suspensions were subjected to sorting by BD Biosciences Aria II Flow Cytometer. Single viable intestinal epithelial cells were gated by forward scatter, side scatter, and by negative staining for DAPI and CD45, and positive staining for EpCAM. Subpopulations were further gated based on CD24 and tdTomato (using R-phycoerythrin/PE channel). Paneth cells (tdT+CD24+) and derivative (tdT+CD24-) cells were FACS-sorted from irradiated (5 days after radiation) and non-irradiated 8-14 week old Lyz1CreER; R26R-tdT mice with one dose of tamoxifen adminstration (10mg/mouse), and subjected to total RNA extraction using Qiagen RNeasy Plus Micro kit.
Paneth Cell Multipotency Induced by Notch Activation following Injury.
Specimen part, Subject
View SamplesAlzheimers disease (AD) is the most common neurodegenerative dementia. Around 10% of cases present an age of onset before 65 years-old, which in turn can be divided in monogenic or familial AD (FAD) and sporadic early-onset AD (EOAD). Mutations in PSEN1, PSEN2 and APP genes have been linked with FAD. The aim of our study was to describe the brain whole-genome RNA expression profile of the posterior cingulate area in EOAD and FAD caused by PSEN1 mutations (FAD-PSEN1). 14 patients (7 EOAD and 7 FAD-PSEN1) and 7 neurologically healthy controls were selected and samples were hybridized in a Human Gene 1.1 microarray from Affymetrix. When comparing controls with EOAD and controls with FAD-PSEN1, we found 3183 and 3351 differentially expressed genes (DEG) respectively (FDR corrected p<0.05). However, any DEG was found in the comparison of the two groups of patients. Microarrays were validated through quantitative-PCR of 17 DEG. In silico analysis of the DEG revealed an alteration in biological pathways related to calcium-signaling, axon guidance and long-term potentiation (LTP), among others, in both groups of patients. These pathways are mainly related with cell signalling cascades, synaptic plasticity and learning and memory processes. In conclusion, the altered biological final pathways in EOAD and FAD-PSEN1 are highly coincident. Also, the findings are in line with those previously reported for late-onset AD (LOAD, onset >65 years-old), which implies that the consequences of the disease at the molecular level are similar in the final stages of the disease.
A preliminary study of the whole-genome expression profile of sporadic and monogenic early-onset Alzheimer's disease.
Sex
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