Gene induction profile among wild-type, NF-IL6KO and KI(LAP) PECs
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE7649 | GEO | 2007/12/05
SECONDARY ACCESSION(S): PRJNA99769
REPOSITORIES: GEO
Similar Datasets
Project description:PECs from wild-type, NF-IL6KO and KI(LAP) mice were stimulated with or without LPS+IFN-gamma for 12h. We used microarrays to check the difference of gene induction among wild type, KO and KI mice. Experiment Overall Design: Peritoneal macrophages were collected for RNA extraction and hybridization on Affymetrix microarrays.
2008-06-15 | E-GEOD-7649 | biostudies-arrayexpress
Project description:Gene induction profile among wild-type, NF-IL6KO and KI(LAP) PECs
| PRJNA99769 | ENA
Project description:Investigation of whole genome gene expression level changes during plant infection in the PecS regulatory mutant compared to the wild type strain. PecS is a global regulator of virulence in D. dadantii and the PecS mutant is hypervirulent.
2017-02-10 | GSE94713 | GEO
Project description:We used RNA-Seq to identify differential gene expression in LAP+ vs. LAP- Gamma-delta T-cells. We report a signature of 407 genes that were enriched in TCRgd+LAP+ vs. TCRgd+LAP- cells with p<0.05. Among the up-regulated genes, we found increased expression of genes related to antigen presentation, including MHC class II molecules (H2-Aa, H2-Ab1, H2-Eb1 and H2-Eb2), CD40 and CD86
2015-09-17 | GSE73077 | GEO
Project description:We used RNA-Seq to identify differential gene expression in LAP+ vs. LAP- Gamma-delta T-cells. We report a signature of 407 genes that were enriched in TCRgd+LAP+ vs. TCRgd+LAP- cells with p<0.05. Among the up-regulated genes, we found increased expression of genes related to antigen presentation, including MHC class II molecules (H2-Aa, H2-Ab1, H2-Eb1 and H2-Eb2), CD40 and CD86 RNA-Seq of TCRgd+LAP+ versus TCRgd+LAP- cells harvested from mouse spleen and Peyer's patches; began with 20 mice for two independent experiments (10 mice each); samples were pooled and for each experiment resulted in one LAP- and one LAP+ sample for RNA-SEQ, or four samples in total; The two LAP+ were combined, resulting in three samples in total for RNA-Seq.
2015-09-17 | E-GEOD-73077 | biostudies-arrayexpress
Project description:Lactiplantibacillus plantarum strain:Lap Genome sequencing
| PRJNA1066604 | ENA
Project description:To analyze the expression profile in the Otx2 knock-in (a knock-in mouse line expressing Otx2 from the Crx locus on chromosome 7) and Crx knockout retina, we performed a microarray analysis using wild-type (Crx +/+), Otx2 KI (Crx Otx2/Otx2) and Crx KO (Crx -/-) retina at P12.
2020-01-24 | GSE129443 | GEO
Project description:BACKGROUND & AIMS: C/EBPbeta is involved in numerous process as carcinogenesis but its role is still not clear due to the existence of an active form (LAP) and an inhibitory form (LIP) of this transcription factor. The main goals of the present research were (i) the identification of genes inversely regulated by LAP and LIP i-e the genuine C/EBPbeta molecular signature in the Hep3B human hepatoma cell line (ii) a better understanding of LAP and LIP respective role in hepatic cells survival and proliferation (iii) the search of the C/EBPbeta signature among hepatocellular carcinomas. METHODS: Using Tet-off expression system we engineered Hep3BLAP and Hep3BLIP cells, in which LAP and LIP were over-expressed respectively. Then, using both expression profiling (DNA arrays) and ChIP-on-chip analysis, we identified genes inversely and/or directly regulated by each of the C/EBPbeta isoforms. The expression levels of these genes regulated by LAP/LIP were compared in controls and HCCs patients. RESULTS: We identified 676 genes inversely regulated by LAP and LIP and among these, 45 are direct targets. Using functional studies, we displayed the opposite role of LAP and LIP in staurosporine-induced cell death and the implication of LAP in the repression of Hep3B cells proliferation. Finally we identified a subgroup of HCCs with a deregulation of 165 genes belonging to C/EBPbeta signature and coding for proteins involved in chemoresistance and metastasis formation. CONCLUSIONS: Our study increases knowledge on LAP and LIP functions and provides first evidence that their molecular signature in the HCCs could predict tumor evolution.
2009-02-27 | GSE15010 | GEO
Project description:Pathogenicity of the phytopathogenic enterobacterium Erwinia chrysanthemi, the causative agent of soft rot disease in many plants, is a complex process involving several factors whose production is subject to temporal regulation during infection. After penetrating into its host plant, E. chrysanthemi resides latently in the plant intercellular spaces without provoking any symptoms, and disease occurs only when the environmental conditions are favourable for massive bacterial multiplication and production of plant cell wall degrading enzymes. PecS is a transcriptional regulator of the MarR family that represses production of plant cell wall degrading enzymes. Here, we used microarray analysis to define the PecS regulon and demonstrated that PecS exerts wide-ranging effects on gene expression in E. chrysanthemi. However, the major effects of PecS are largely confined to specific genes that could be linked to pathogenicity and to a group of genes concerned with evading host defences. Among the identified targets are the genes encoding plant cell wall degrading enzymes, secretion systems, the genes involved in flagella synthesis, in biosurfactant synthesis, in oxidative stress response as well as genes encoding toxin-like virulence factors such as NipE and Hemolysin-coregulated proteins. Electromobility shift assays and DNAse I footprinting demonstrated that PecS directly interacts with the regulatory regions of five new targets, ahpC, rhlA, nipE, virK, avrL, that define three different functional classes of genes: oxidative stress response genes (ahpC), biosurfactant synthesis gene (rhlA), genes encoding exported proteins related to other plant associated bacteria proteins (nipE, virK, avrL). Based on this work, we propose a pivotal role of PecS in the switch from a saprophytic to a parasitic lifestyle.
2008-10-09 | E-TABM-428 | biostudies-arrayexpress
Project description:BACKGROUND & AIMS: C/EBPbeta is involved in numerous process as carcinogenesis but its role is still not clear due to the existence of an active form (LAP) and an inhibitory form (LIP) of this transcription factor. The main goals of the present research were (i) the identification of genes inversely regulated by LAP and LIP i-e the genuine C/EBPbeta molecular signature in the Hep3B human hepatoma cell line (ii) a better understanding of LAP and LIP respective role in hepatic cells survival and proliferation (iii) the search of the C/EBPbeta signature among hepatocellular carcinomas. METHODS: Using Tet-off expression system we engineered Hep3BLAP and Hep3BLIP cells, in which LAP and LIP were over-expressed respectively. Then, using both expression profiling (DNA arrays) and ChIP-on-chip analysis, we identified genes inversely and/or directly regulated by each of the C/EBPbeta isoforms. The expression levels of these genes regulated by LAP/LIP were compared in controls and HCCs patients. RESULTS: We identified 676 genes inversely regulated by LAP and LIP and among these, 45 are direct targets. Using functional studies, we displayed the opposite role of LAP and LIP in staurosporine-induced cell death and the implication of LAP in the repression of Hep3B cells proliferation. Finally we identified a subgroup of HCCs with a deregulation of 165 genes belonging to C/EBPbeta signature and coding for proteins involved in chemoresistance and metastasis formation. CONCLUSIONS: Our study increases knowledge on LAP and LIP functions and provides first evidence that their molecular signature in the HCCs could predict tumor evolution. Total genomic DNA were extracted from 3 Hep3BLAP expressing LAP and were labelled Cy3 fluorochrome. Genomic DNA were extracted from 3 Hep3BLAP expressing LAP, were immunoprecipited with anti-CEBPbeta antibody and were labelled with Cy5 fluorochrome. Each sample was hybridized on an Agilent two-color microarray G4489A (Human Promoter ChIP-on-Chip Set 244K).
2010-05-22 | E-GEOD-15010 | biostudies-arrayexpress