This SuperSeries is composed of the SubSeries listed below.
Genomic characterization of liver metastases from colorectal cancer patients.
Sex, Age, Disease, Disease stage
View SamplesTo determine whether an accelerated aging-like phenotype occurs in hematopoiesis of young Tif1?-/- mice (4 months old), we purified 200,000 hematopoietic stem cells (LSK: Lineage negative, Sca1+, c-Kit+) from Tif1?-/- mice and performed high-throughput mRNA sequencing (RNA-seq). We compared this transcriptome to physiological aging by creating two other RNAseq libraries from young (4 months old) and old (20 months old) wild type mice. Overall design: RNAseq study on young Tif1?-/- mice (4 months old), young wild type mice (4 months old) and old wild type mice (20 months old).
Tif1γ regulates the TGF-β1 receptor and promotes physiological aging of hematopoietic stem cells.
No sample metadata fields
View SamplesTo explore events that govern the differentiation of human nave B cells (NBCs) into memory B cells and plasma cells (PCs), we designed an in vitro 2-step culture model leading non-switched NBC precursors to differentiate into two cell compartments: CD20loCD38hi and CD20+CD38+.
IL-2 requirement for human plasma cell generation: coupling differentiation and proliferation by enhancing MAPK-ERK signaling.
Specimen part, Subject, Time
View SamplesFanconi anemia (FA) is a genetic disorder characterized by congenital abnormalities, bone marrow failure and increased susceptibility to cancer. Of the fifteen FA proteins, Fanconi anemia group C (FANCC) is one of eight FA core complex components of the FA pathway. Unlike other FA core complex proteins, FANCC is mainly localized in the cytoplasm, where it is thought to function in apoptosis, redox regulation, cytokine signaling and other processes. Previously, we showed that regulation of FANCC involved proteolytic processing during apoptosis. To elucidate the biological significance of this proteolytic modification, we searched for molecular interacting partners of proteolytic FANCC fragments. Among the candidates obtained, the transcriptional corepressor protein C-terminal binding protein-1 (CtBP1) interacted directly with FANCC and other FA core complex proteins. Although not required for stability of the FA core complex or ubiquitin ligase activity, CtBP1 is essential for proliferation, cell survival and maintenance of chromosomal integrity. Expression profiling of CtBP1-depleted and FA-depleted cells revealed that several genes were commonly up- and down-regulated, including the Wnt antagonist Dickkopf-1 (DKK1). These findings suggest that FA and Wnt signaling via CtBP1 could share common effectors.
Fanconi anemia proteins interact with CtBP1 and modulate the expression of the Wnt antagonist Dickkopf-1.
Cell line
View SamplesAnalysis of the transcriptome of -catenin flox/- mES cells in comparison with -catenin null mES cells or -catenin null mES cells stably transfected with an E-cadherin--catenin fusion protein.
E-cadherin is required for the proper activation of the Lifr/Gp130 signaling pathway in mouse embryonic stem cells.
Specimen part
View SamplesRelatively little is understood about the dynamics of global hostpathogen transcriptome changes that occur during bacterial infection of mucosal surfaces. To test the hypothesis that group A Streptococcus (GAS) infection of the oropharynx provokes a host transcriptome response, we performed genome-wide transcriptome analysis using a nonhuman primate model of experimental pharyngitis. We also identified host and pathogen biological processes and individual host and pathogen gene pairs with correlated patterns of expression, suggesting interaction. For this study, 509 host genes and seven biological pathways were differentially expressed throughout the entire 32-day infection cycle. GAS infection produced an initial widespread significant decrease in expression of many host genes, including those involved in cytokine production, vesicle formation, metabolism, and signal transduction. This repression lasted until day 4, at which time a large increase in expression of host genes was observed, including those involved in protein translation, antigen presentation, and GTP-mediated signaling. The interactome analysis identified 73 host and pathogen gene pairs with correlated expression levels. We discovered significant correlations between transcripts of GAS genes involved in hyaluronic capsule production and host endocytic vesicle formation, GAS GTPases and host fibrinolytic genes, and GAS response to interaction with neutrophils. We also identified a strong signal, suggesting interaction between host T cells and genes in the GAS mevalonic acid synthesis pathway responsible for production of isopentenyl-pyrophosphate, a short-chain phospholipid that stimulates these T cells. Taken together, our Q:2 results are unique in providing a comprehensive understanding of the hostpathogen interactome during mucosal infection by a bacterial pathogen.
Interactome analysis of longitudinal pharyngeal infection of cynomolgus macaques by group A Streptococcus.
Sex, Subject
View SamplesIn this work we present the PrPC-dependent gene expression signature in N2A cells and its implication on the most overrepresented functions; cell cycle, cell growth and proliferation and cell morphology.
PrP(C) regulates epidermal growth factor receptor function and cell shape dynamics in Neuro2a cells.
Specimen part
View SamplesIn the present study, we investigated the consequences of n-3 polyunsaturated fatty acids (PUFA) depletion on hepatic lipid metabolism in mice fed during three months with a diet presenting a high n-6/n-3 PUFA ratio to induce n-3 PUFA depletion. Microarray analyses were performed to identify the molecular targets involved in the development of hepatic steatosis associated with n-3 PUFA depletion.
Hepatic n-3 polyunsaturated fatty acid depletion promotes steatosis and insulin resistance in mice: genomic analysis of cellular targets.
Sex, Specimen part, Treatment
View SamplesWe have generated mouse models of real CMT1B mutations in the gene encoding for myelin protein zero (P0). One of these mutants, P0S63del is retained in the ER where it elicits an unfolded protein response (UPR). Genetic ablation of the UPR factor CHOP restores the motor capacity in S63del mice. We used microarray to decipher the molecular mechanism undelying the P0S63del neuropathy and the rescue in S63del/Chop null nerves.
Resetting translational homeostasis restores myelination in Charcot-Marie-Tooth disease type 1B mice.
Age, Specimen part
View SamplesEffect on the transcriptome of an insertion in the gene At3g08610 encoding a subunit of mitochondrial complex I
Remodeled respiration in ndufs4 with low phosphorylation efficiency suppresses Arabidopsis germination and growth and alters control of metabolism at night.
Age, Specimen part, Time
View Samples