Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA179283 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE42174: Global expression analysis of DLBCL cell lines with LITAF over-expression or silencing GSE42203: Global expression analysis of DLBCL and SMZL cell lines Refer to individual Series
2012-11-10 | E-GEOD-42204 | biostudies-arrayexpress
Project description:Global expression analysis of DLBCL cell lines with LITAF over-expression or silencing
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Project description:The multifunctional protein lipopolysaccharide-induced TNFalpha factor (LITAF) induces the secretion of inflammatory cytokines in monocytes and regulates protein degradation in neural cells. In B-cell lymphomas, LITAF is frequently inactivated by epigenetic mechanisms, but beyond these data little is known about its regulation and function. Immunohistochemical and gene expression profiling analyses of normal and malignant B-cells revealed that LITAF and BCL6 exhibited opposite expression patterns. Accordingly, chromatin immunoprecipitation and luciferase experiments showed that LITAF is transcriptionally repressed by BCL6 in germinal center (GC) lymphocytes and in B-cell lymphoma cells. Gain- and-loss-of-function assays demonstrated that LITAF does not exert any of its previous roles. Conversely, LITAF co-localized with autophagosomes in B-cells whereby activated autophagic responses, which were abrogated upon LITAF silencing. Therefore, BCL6-mediated transcriptional repression of LITAF may contribute to an appropriate GC reaction by suppressing autophagy in GC lymphocytes, whereas constitutive repression of autophagic responses may promote B-cell lymphoma development. Analysis of global gene expression in the diffuse large B-cell lymphoma (DLBCL) cell lines KARPAS-231 and VAL treated with a specific siRNA for LITAF or a scrambled control, and analysis of global gene expression in the DLBCL cell lines RL and SC-1 stably transfected with a tetracycline-inducible LITAF expression vector in the presence or absence of 4 mg/ml doxycycline in the culture medium. The over-expression experiments were performed in duplicate and the silencing experiments in triplicate, resulting in a total of 20 microarrays.
2012-11-10 | E-GEOD-42174 | biostudies-arrayexpress
Project description:The multifunctional protein lipopolysaccharide-induced TNFalpha factor (LITAF) induces the secretion of inflammatory cytokines in monocytes and regulates protein degradation in neural cells. In B-cell lymphomas, LITAF is frequently inactivated by epigenetic mechanisms, but beyond these data little is known about its regulation and function. Immunohistochemical and gene expression profiling analyses of normal and malignant B-cells revealed that LITAF and BCL6 exhibited opposite expression patterns. Accordingly, chromatin immunoprecipitation and luciferase experiments showed that LITAF is transcriptionally repressed by BCL6 in germinal center (GC) lymphocytes and in B-cell lymphoma cells. Gain- and-loss-of-function assays demonstrated that LITAF does not exert any of its previous roles. Conversely, LITAF co-localized with autophagosomes in B-cells whereby activated autophagic responses, which were abrogated upon LITAF silencing. Therefore, BCL6-mediated transcriptional repression of LITAF may contribute to an appropriate GC reaction by suppressing autophagy in GC lymphocytes, whereas constitutive repression of autophagic responses may promote B-cell lymphoma development. 40 diffuse large B-cell lymphoma (DLBCL) and 3 splenic marginal zone lymphoma (SMZL) untreated cell lines were analyzed for global gene expression with the GeneChip® Human Genome U133 Plus 2.0 Array (Affymetrix). SMZL cell lines were hybridized in duplicate, resulting in a total of 46 microarrays.
2012-11-10 | E-GEOD-42203 | biostudies-arrayexpress
Project description:Global expression analysis of DLBCL and SMZL cell lines
| PRJNA179286 | ENA
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Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression. Two-condition experiment, Normoxic MSCs vs. Hypoxic MSCs.
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