Tankyrase enhances beta-catenin signaling via PARsylation and subsequent degradation of Axin, a negative regulator of beta-catenin. Tankyrase inhibitors stabilize Axin and suppress beta-catenin signaling. We developed a novel tankyrase inhibitor, RK-287107.
RK-287107, a potent and specific tankyrase inhibitor, blocks colorectal cancer cell growth in a preclinical model.
Specimen part, Treatment
View Samplesgenes regualted by LPS or LPS+cAMP stimulation in BMDCs
Cyclic adenosine monophosphate suppresses the transcription of proinflammatory cytokines via the phosphorylated c-Fos protein.
Specimen part
View SamplesTranscriptome analysis of the effect of RECTAS on fibroblast cells derived from a familial dysautonomia patient.
Rectifier of aberrant mRNA splicing recovers tRNA modification in familial dysautonomia.
Specimen part, Treatment
View SamplesRNA-Seq analysis of SSA treated cells Overall design: HeLa cells, nuclear and cytoplasmic fractions, treated with SSA or MeOH
Global analysis of pre-mRNA subcellular localization following splicing inhibition by spliceostatin A.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The transcriptional regulator Aire binds to and activates super-enhancers.
Sex, Age, Specimen part, Treatment
View SamplesMicroarray profiles of MECs from mice treated with topoisomerase inhibitors
The transcriptional regulator Aire binds to and activates super-enhancers.
Sex, Age, Treatment
View SamplesTo identify gene expression profile changes upon SNRNP40 depletion, RNA-sequencing was performed on breast cancer cells transfected with siRNAs targeting SNRNP40. Overall design: Libraries were generated using ScriptSeq v2 RNA-seq Library Preparation Kit (Epicentre) and run on Illumina HiSeq 2500.
Highly variable cancer subpopulations that exhibit enhanced transcriptome variability and metastatic fitness.
No sample metadata fields
View SamplesSevere acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes an immune-mediated disease. We have recently shown that SARS-CoV-induced epithelial Calu-3 cytokines could exacerbate and dampen host inflammatory and T cell responses, respectively, through modulating the functions of macrophages and dendritic cells, thereby suggesting that not only are lung epithelial cells the primary cells of SARS-CoV infection, but they also involve in initiating and orchestrating the host innate and adaptive immunity. Comprehensive evaluation of the complex epithelial signaling to SARS-CoV is, thus, crucial for paving the way to better understand SARS pathogenesis and develop the innovative therapeutics against SARS. Here, based on the microarray-based functional genomics, we reported that 2B4 cells, a clonal derivative of Calu-3 cells, elicited a temporal and spatial activation of nuclear factor (NF)kappaB, activator protein (AP)-1 (ATF2/c-Jun), and interferon regulatory factor (IRF)-3/-7 at 12-, 24-, and 48-hrs post infection (p.i.), respectively, resulting in the activation of many antiviral genes, including interferon (IFN)-, -s, SARS-related inflammatory mediators, and various IFN-stimulated genes (ISGs). While elevated responses of IFN- and IFN-s were not detected until 48-hrs p.i., as a consequence of a delayed IRF-3/-7 activation, we showed, for the first time, that both types of IFNs exerted previously under-described non-redundant, complementary, and/or synergistic effects on the epithelial defense against SARS-CoV. Collectively, our results highlight the molecular mechanisms of the sequential activation of virus- and IFN-dependent signaling of lung epithelial cells against SARS-CoV and identify novel cellular targets for future studies, aiming at advancing strategies against SARS.
Dynamic innate immune responses of human bronchial epithelial cells to severe acute respiratory syndrome-associated coronavirus infection.
Cell line, Time
View SamplesAnalysis of gene expressions in human microvascular endothelial cells (HMVEC)s following co-cultured with mouse dorsal root ganglion cells. Results provide insight into a role for responses of neurovascular interaction in endothelial cell in angiogenesis and vascular remodeling.
JunB regulates angiogenesis and neurovascular parallel alignment in mouse embryonic skin.
Specimen part
View SamplesAnalysis of gene expression in immortalized human microvascular endothelial cells (TIME cells) following forced expression of the JunB. Results provide insight into a role for the JunB signaling pathway in endothelial cell.
JunB regulates angiogenesis and neurovascular parallel alignment in mouse embryonic skin.
Specimen part
View Samples