Seedlings 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 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 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 SamplesThe MYC transcription factor is a master regulator of diverse cancer pathways and somatic cell reprogramming. MYC is a compelling therapeutic target that exhibits cancer-specific cellular effects. Pharmacologic inhibition of MYC function has proven challenging due to its numerous modes of forced expression and the difficulty of disrupting protein-DNA interactions. Here we demonstrate the rapid and potent abrogation of MYC gene transcription by representative small molecule bromodomain inhibitors of the BET family of chromatin adaptors. This transcriptional suppression of MYC was observed in the context of the natural, chromosomally translocated, and amplified gene locus. Inhibition of BET bromodomain-promoter interactions and subsequent reduction of MYC transcript and protein levels resulted in G1 arrest and extensive apoptosis in a variety of leukemia and lymphoma cell lines. Exogenous expression of MYC from an artificial promoter that is resistant to BET regulation significantly protected cells from growth suppression by BET inhibitors and revealed that MYC exerts a direct and tight control of key pro-growth and anti-apoptotic target genes. Transcriptional profiling of two cells after 4 and 8 hours of treatment with BET inhibitor shows that both MYC and its targets are strongly down-regulated. We thus demonstrate that pharmacologic inhibition of MYC is achievable through targeting BET bromodomains, and suggest that such inhibitors may have broad clinical applicability given the widespread pathogenetic role of MYC in cancer.
Targeting MYC dependence in cancer by inhibiting BET bromodomains.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve.
Age, Specimen part, Treatment
View SamplesSpiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves.
Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve.
Specimen part
View SamplesSpiral ganglion neurons (SGNs) and the associated components of the auditory nerve are primary carriers of auditory information from hair cells to the brain. Loss of SGNs occurs with many pathological conditions, resulting in permanent sensorineural hearing loss. Neural stem/progenitors (NSPs) have been well-characterized in several locations of adult brain and retina. However, it is unclear whether NSPs are present in the adult auditory nerve. Here we examined the self-renewal potential of the adult auditory nerve using ouabain application as a well-established mouse model of acute SGN injury. The observed increase in cell proliferation, alteration in enchromatin/heterochromatin ratio and down-regulation of histone deacetylase expression in glial cells suggest that the quiescent glial cells convert to an activated state after SGN degeneration. This was further confirmed by global gene expression analysis of injured auditory nerves, which showed up-regulation of numerous neurogenesis- and/or development-associated genes shortly after ouabain exposure. These genes include molecular markers commonly used for the identification of NSPs. Under a strict culture regimen, auditory nerve-derived cells of adult mouse ears gave rise to neurospheres, suggesting that multipotent NSPs are present in adult cochlear nerve. Neurosphere assays on Sox2 transgenic mice revealed that Sox2+ glial cells are the source for NSPs. Our data also showed that acute injury or hypoxia enhances neurosphere formation. Taken together, our study revealed that glial cells of adult cochlea exhibit several NSP characteristics, and hence these mature non-neuronal cells may be important targets for promoting self-repair of degenerative auditory nerves.
Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve.
Specimen part
View Samples