Adenovirus infection leads to increased glycolytic metabolism in host cells. Expression of a single gene product encoded within the E4 early transcription region, E4ORF1, is sufficient to promote increased glycolytic flux in cultured epithelial cells.
Adenovirus E4ORF1-induced MYC activation promotes host cell anabolic glucose metabolism and virus replication.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Regulatory T Cells Orchestrate Similar Immune Evasion of Fetuses and Tumors in Mice.
Age, Specimen part
View SamplesAnalysis of uterine microenvironment at gene expression level. The hypothesis tested in the present study was that Tregs orchestrated the immune reponse triggered in presence of embryo
Regulatory T Cells Orchestrate Similar Immune Evasion of Fetuses and Tumors in Mice.
Age, Specimen part
View SamplesAnalysis of B16 tumor microenvironment at gene expression level. The hypothesis tested in the present study was that Tregs orchastrated the immune reponse triggered in presence of tumors
Regulatory T Cells Orchestrate Similar Immune Evasion of Fetuses and Tumors in Mice.
Age, Specimen part
View SamplesAnalysis of uterine microenvironment at gene expression level. The hypothesis tested in the present study was that Tregs orchestrated the immune reponse triggered in presence of embryo.
Regulatory T Cells Orchestrate Similar Immune Evasion of Fetuses and Tumors in Mice.
Age, Specimen part
View SamplesSPT6, encoded by the SUPT6H in humans and Supt6 in mice, respectively, is a conserved histone chaperone that interacts with RNA polymerase II and participates in transcription elongation. However, the question of how SPT6 comes into play in transcriptional activation upon signaling, particularly in mammalian cells, has remained elusive. We investigated the contribution of SPT6 to interferon beta (IFNbeta) induced transcription in mouse NIH3T3 cells. IFNbeta triggers rapid and high level transcription of many IFN-stimulated genes (ISGs). We report here that SPT6 is recruited to ISGs after IFN stimulation. This recruitment was dependent on the interaction with the methyltransferase, NSD2. Further, siRNA-based SPT6 knockdown reduced levels of ISG activation. RNA-Seq analysis showed that SPT6 knockdown diminished about 50% of ISGs whose induction levels were higher than those unaffected by SPT6 knockdown. Under the tested conditions, SPT6 knockdown did not measurably change expression of constitutively expressed genes. This report highlights that SPT6 is recruited in a stimulus-dependent manner and elicits a major impact on signal induced transcription. Overall design: RNA-seq of NIH3T3 cells.
SPT6 interacts with NSD2 and facilitates interferon-induced transcription.
Cell line, Treatment, Subject
View SamplesWe report that combining NGN2 programming with SMAD and WNT inhibition generates patterned induced neurons (hpiNs).Transcriptional analyses showed that hpiN cultures contained cells along a developmental continuumranging from poorly differentiated neuronal progenitors to well-differentiated, excitatory glutamatergic neurons. The most differentiated neurons could be identified using a CAMK2A::GFP reporter gene. Overall design: RNA sequencing analysis (population and single cell) over hpiNs differentiation time (D0 through D49 after induction). Two independent iPS lines, 9 time points, three replicates each.
Combining NGN2 Programming with Developmental Patterning Generates Human Excitatory Neurons with NMDAR-Mediated Synaptic Transmission.
Specimen part, Disease, Cell line, Subject, Time
View SamplesInnate immune memory is a vital mechanism of myeloid cell plasticity that occurs in response to environmental stimuli and alters subsequent immune responses. Two types of immunological imprinting can be distinguished—training and tolerance. These are epigenetically mediated and enhance or suppress subsequent inflammation, respectively. Whether immune memory occurs in tissue-resident macrophages in vivo and how it may affect pathology remains largely unknown. Here we demonstrate that peripherally applied inflammatory stimuli induce acute immune training and tolerance in the brain and lead to differential epigenetic reprogramming of brain-resident macrophages (microglia) that persists for at least six months. Strikingly, in a mouse model of Alzheimer's pathology, immune training exacerbates cerebral beta-amyloidosis and immune tolerance alleviates it; similarly, peripheral immune stimulation modifies pathological features after stroke. Our results identify immune memory in the brain as an important modifier of neuropathology. Overall design: mRNA was isolated from FACS-purified microglia and prepared for RNA-sequencing.
Innate immune memory in the brain shapes neurological disease hallmarks.
Sex, Specimen part, Treatment, Subject
View SamplesThe Collaborative Cross (CC) recombinant inbred panel was conceived as an ideal resource for mammalian system genetics. The pre-CC is a proof-of-concept experiment involving CC lines that have undergone at least five generations of inbreeding. Siblings from these lines were each involved in one of four distinct phenotyping arms, then genotyped on a high-density Affymetrix platform. The genetic profile of these emerging lines reveals high diversity, balanced allele frequencies, and well-distributed recombination all ideal qualities for a mapping panel. We have mapped white spot, a discrete trait; body weight, a highly polygenic complex trait; and more than 11,000 liver gene expression traits. These analyses provide a glimpse of the potential mapping power and resolution of the CC.
Genetic analysis of complex traits in the emerging Collaborative Cross.
Specimen part
View Samples