Expression profiling of Xenografts of Hepatocellular Carcinoma
Bevacizumab and rapamycin induce growth suppression in mouse models of hepatocellular carcinoma.
Specimen part
View SamplesFunctional characterization of human dendritic cell subsets is limited due to the very low frequency of these cells in vivo. We developed an in vitro culture system for the simultaneous generation of XCR1+ DCs and MoDCs from cord blood CD34+ cells. Their global gene expression profiles at steady state and under activation, phenotypes, morphologies and responses to different TLR ligands where characterized and compared with those of their in vivo counterparts. The study demonstrated that the XCR1+ DCs generated in vitro from cord blood CD34+ cells are equivalent to blood XCR1+ DCs and also allowed a rigorous comparison of this DC subset with MoDC which are often considered as the reference model for DCs. Altogether, our results showed that in vitro generated XCR1+ DCs are a better model for the study of blood DC than the conventionally used MoDCs.
Human XCR1+ dendritic cells derived in vitro from CD34+ progenitors closely resemble blood dendritic cells, including their adjuvant responsiveness, contrary to monocyte-derived dendritic cells.
Specimen part, Treatment
View SamplesGibberellin mobilizes distinct DELLA-dependent transcriptomes to regulate seed germination and floral development in Arabidopsis
Gibberellin mobilizes distinct DELLA-dependent transcriptomes to regulate seed germination and floral development in Arabidopsis.
Specimen part
View SamplesHomeostasis of the gut microbiota is pivotal to the survival of the host. Intestinal T cells and Innate Lymphoid cells (ILCs) control the composition of the microbiota and respond to its perturbations. Interleukin 22 (IL-22) plays a pivotal role in the immune control of gut commensal and pathogenic bacteria and is secreted by a heterogeneous population of intestinal T cells, NCR- ILC3 and NCR+ILC3. Expression of NCR by ILC3 is believed to define an irreversible effector ILC3 end-state fate in which these cells are key to control of bacterial infection via their production of IL-22. Here we identify the core transcriptional signature that drives the differentiation of NCR- ILC3 into NCR+ ILC3 and reveal that NCR+ILC3 exhibit more plasticity than originally thought, as NCR+ ILC3 can revert to NCR- ILC3. Contrary to the prevailing understanding of NCR+ ILC3 genesis and function, in vivo analyses of mice conditionally deleted of the key ILC3 genes Stat3, Il22, Tbet and Mcl1 demonstrated that NCR+ ILC3 were not essential for the control of colonic infections in the presence of T cells. However, NCR+ ILC3 were mandatory for homeostasis of the caecum. Our data identify that the interplay of intestinal T cells and ILC3 results in robust complementary fail-safe mechanisms that ensure gut homeostasis. Overall design: Transcriptional profiling of wild-type and T-bet knockout innate lymphoid cells (ILC3) using RNA sequencing
Complementarity and redundancy of IL-22-producing innate lymphoid cells.
Specimen part, Cell line, Subject
View SamplesLiver RNA was collected from three genotypes: WT controls, KCP knockout (KCP-KO) mutants, and KCP-Transgenic (KCP-Tg) overexpressing mice.
The kielin/chordin-like protein KCP attenuates nonalcoholic fatty liver disease in mice.
Specimen part
View SamplesES cells are able to self-renew and remain pluripotent. These characteristics are maintained by both genetic and epigenetic regulators. Protein arginine methyltransferase (PRMT) 4 and 5 are shown to be important in early embryonic development and in ES cells. PRMT6-mediated di-methylation of histone H3 at arginine 2 (H3R2me2) can antagonize the tri-methylation of histone H3 at lysine 4, which marks active genes. However, it is unclear whether PRMT6 and PRMT6-mediated H3R2me2 play crucial roles in early embryonic development and ES cell identity. In this study, we investigate their functions using mouse ES cells as the model.
Protein arginine methyltransferase 6 regulates embryonic stem cell identity.
Cell line
View SamplesIdentifying PDEF regulated genes may shed light on the mechanism by which PDEF may induce breast cancer progression. To that purpose, we have used the MCF-7 human breast tumor cell line model to identify PDEF induced genes. Briefly, PDEF expression was down regulated by shRNA in MCF-7 cells and RNA probes from PDEF-down regulated and control MCF-7 cells were used to screen the Affymetrics HG-U133A Gene Chips. This analysis found 62 genes that were induced 2-fold or higher by PDEF. Further analysis of 3 of these genes namely S100A7, CEACAM6 and B7-H4 in primary breast tumors showed CEACAM6 as a frequently elevated and co-exressed gene with PDEF in these tumors.
Prostate derived Ets transcription factor and Carcinoembryonic antigen related cell adhesion molecule 6 constitute a highly active oncogenic axis in breast cancer.
Cell line
View SamplesTo understand the transcriptional program controlled by AGL24, we took advantage of a functional estradiol-inducible AGL24 expression system in combination with microarray analysis to identify AGL24 target genes.
Direct interaction of AGL24 and SOC1 integrates flowering signals in Arabidopsis.
No sample metadata fields
View SamplesThe complex milieu of inflammatory mediators associated with many diseases is often too dilute to directly measure in the periphery, necessitating development of more sensitive measurements suitable for mechanistic studies, earlier diagnosis, guiding selection of therapy, and monitoring interventions. Previously, we determined that plasma of recent-onset (RO) Type 1 diabetes (T1D) patients induce a proinflammatory transcriptional signature in fresh peripheral blood mononuclear cells (PBMC) relative to that of unrelated healthy controls (HC). Here, using an optimized cryopreserved PBMC-based protocol, we apply this approach to inflammatory bowel disease by examining groups of Crohn's disease (CD) and ulcerative colitus (UC) patients. The induced plasma induced signatures are compared to those of Type 1 diabetes patients (RO T1D) as well as unrelated healthy controls (uHC).
Plasma-induced signatures reveal an extracellular milieu possessing an immunoregulatory bias in treatment-naive paediatric inflammatory bowel disease.
No sample metadata fields
View SamplesThe aim of present study was to describe the genetic pathways activated during the community acquired bacterial meningitis (BM) by using genome-wide RNA expression profiling combined with functional annotation of transcriptional changes. We included 21 patients with BM hospitalized in 2008. The control group consisted of 18 healthy subjects. The RNA was extracted from whole blood, globin mRNA was depleted and gene expression profiling was performed with GeneChip Human Gene 1.0 ST Arrays enabling the analysis of 28,869 genes. Gene expression profile data were analyzed using Bioconductor packages and Bayesian modeling. Functional annotation of the enriched gene sets was used to define changed genetic networks. We also analyzed if the gene expression profile depends on the clinical course and outcome. In order to verify the genechip results, we chose ten functionally relevant genes with high statistical significance (CD177, IL1R2, IL18R1, IL18RAP, OLFM4, TLR5, CPA3, FCER1A, IL5RA, IL7R) and performed quantitative real-time (qRT) PCR.We identified the significant differences at p values of <0.05 in 8569 genes and after False Discovery Rate (FDR) correction, total of 5500 genes remained significant at p value of <0.01. Quantitative RT-PCR confirmed differential expression for selected genes. Functional annotation and network analysis indicated that most of the genes were related to activation of humoral and cellular immune responses (enrichment score 43). Those changes were found in adults and in children with BM compared to the healthy controls. Gene expression profile didnt depend on the clinical outcome, but there was very strong influence by the type of the pathogen. This study demonstrates a strong functional genomic evidence of the over-active immune response during bacterial meningitis. This hyperactive response possibly explains the complicated clinical course of this disease.
Peripheral blood RNA gene expression profiling in patients with bacterial meningitis.
Specimen part
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