RNA-Seq profiling of MCF-7 and MDA-MB-231. We profiled RNA expression in the estrogen-receptor-positive (ER+) MCF-7 and the triple-negative MDA-MB-231 breast cancer cells. The objective was to find genes differentially expressed between these cell lines as potential drivers of invasiveness of the triple-negative MDA-MB-231. We further utilized the identified differential genes to validate expression-responsive module of non-canonical Wnt signaling pathway. Overall design: 2 biological replicates of MCF-7 and 3 biological replicates of MDA-MB-231
Newly Constructed Network Models of Different WNT Signaling Cascades Applied to Breast Cancer Expression Data.
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View SamplesRNA-Seq profiling of estrogen-receptor-positive MCF-7 cell lines with different perturbations of non-canonical WNT signaling . The MCF-7 cells were either transfected with an empty vector (pcDNA) or with a ROR2 overexpression construct, in parallel with or without stimulation with recombinant WNT5A. The objective was to find expression-responsive targets of these perturbations as potential drivers of increased cell invasiveness. Overall design: Four conditions of MCF-7 cells each in 3 replicates: 1. empty vector (pcDNA), 2. empty vector (pcDNA) with WNT5A stimulation, 3. ROR2 overexpression construct, 4. ROR2 overexpression construct with WNT5A stimulation
Ror2 Signaling and Its Relevance in Breast Cancer Progression.
No sample metadata fields
View SamplesRecently global gene expression profiling of patients samples lead to a molecular definition of Burkitt Lymphoma (BL) with lymphocyte enhancer-binding factor 1 (LEF1) as a signature gene. Here we report the discovery of nucleic LEF1 in a very high proportion of BL cases (15/18) and LEF1 target genes. Germinal center B cells were devoid of detectable nuclear LEF1 expression as mantle cell lymphoma (0/5), marginal zone lymphoma (0/6), follicular lymphoma (0/12) or diffuse large B cell lymphoma (DLBCL) (1/31). Using whole genome gene expression profiling after transient knockdown of LEF1 in BL cell lines, new LEF1 target genes were identified. The joint expression of these genes in primary BL samples shows that LEF1 is not only expressed aberrantly in BL but also transcriptionally active. Our study identified aberrantly expressed LEF1 and its target genes suggesting an important functional role in BLs.
Aberrant lymphocyte enhancer-binding factor 1 expression is characteristic for sporadic Burkitt's lymphoma.
Cell line
View SamplesMicroarray analysis of 28 brain metastasis samples from lung adenocarcinoma patients.
Isolated metastasis of an EGFR-L858R-mutated NSCLC of the meninges: the potential impact of CXCL12/CXCR4 axis in EGFR<sub>mut</sub> NSCLC in diagnosis, follow-up and treatment.
No sample metadata fields
View SamplesN2 young adult animals were analyzed four hours after exposure to wild-type Candida albicans DAY185, heat-killed C. albicans DAY185 and heat-killed Escherichia coli OP50, all on Brain Heart Infusion (BHI) agar. It was necessary to use heat-killed E. coli OP50 as a control for these experiments because live E. coli OP50 (the normal nematode food source) is pathogenic to nematodes on BHI agar. These data identify the C. elegans genes that are differentially regulated during nematode infection with a human fungal pathogen.
Candida albicans infection of Caenorhabditis elegans induces antifungal immune defenses.
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View SamplesThe nematode Caenorhabditis elegans offers currently untapped potential for carrying out high-throughput, live-animal screens of low molecular weight compound libraries to identify molecules that target a variety of cellular processes. We previously used a bacterial infection assay in C. elegans to identify 119 compounds that affect host-microbe interactions among 37,214 tested. We subsequently found that one of these small molecules, RPW-24, protects C. elegans from bacterial infection by stimulating the host immune response of the nematode. Using transcriptome profiling, epistasis pathway analyses with C. elegans mutants, and an RNAi screen, we showed that RPW-24 promotes resistance to Pseudomonas aeruginosa infection by inducing the transcription of a remarkably small number of C. elegans genes (~1.3% of all genes) in a manner that partially depends on the evolutionarily-conserved p38 MAP kinase pathway and the transcription factor ATF-7. These data demonstrated that the immunostimulatory activity of RPW-24 is required for its efficacy and define a novel C. elegans-based strategy to identify compounds with activity against antibiotic-resistant bacterial pathogens. Here we present the microarray data that were used to define the genes that are differentially regulated in wild-type nematodes following exposure to RPW-24.
Stimulation of host immune defenses by a small molecule protects C. elegans from bacterial infection.
Specimen part, Treatment
View SamplesZIP-3 has been shown to repress the mitochondrial-UPR response. To identify genes repressed by ZIP-3, we compared transcript profiles from wildtype, atfs-1(tm4919) and zip-3(gk3164) worms raised on control RNAi or spg-7 RNAi Overall design: RNA samples were prepared from wild-type(wt) and zip-3(gk3164)(mutant) worms fed either control RNAi or spg-7 RNAi. Worms were synchronized by bleaching, raised on NGM plates seeded with control RNAi or spg-7 RNAi till L4 stage and then harvested. Each experiment was performed in triplicate indicated as 1,2 and 3.
Mitochondrial UPR repression during <i>Pseudomonas aeruginosa</i> infection requires the bZIP protein ZIP-3.
Specimen part, Subject
View SamplesZIP-3 has been shown to repress the mitochondrial-UPR genes and immune response during P. aeruginosa infection. To identify genes repressed by ZIP-3, we compared transcript profiles from wildtype and zip-3(gk3164) worms raised on P. aeruginosa or E. coli. Overall design: RNA samples were prepared from wild-type(wt) and zip-3(gk3164)(mutant) worms fed either E. coli or P. aeruginosa. Worms were synchronized by bleaching, starved on empty NGM plates for 48h, transferred to E. coli or P. aeruginosa seeded NGM plates for 18h and then harvested. Each experiment was performed in triplicate indicated as 1,2 and 3.
Mitochondrial UPR repression during <i>Pseudomonas aeruginosa</i> infection requires the bZIP protein ZIP-3.
Specimen part, Subject
View SamplesMicrophthalmos is a rare congenital anomaly characterized by reduced eye size and visual deficits of variable degrees. Sporadic and hereditary microphthalmos has been associated to heterozygous mutations in genes fundamental for eye development. Yet, many cases are idiopathic or await the identification of molecular causes. Here we show that haploinsufficiency of Meis1, a transcription factor with an evolutionary conserved expression in the embryonic trunk, brain and sensory organs, including the eye, causes microphthalmic traits and visual impairment, in adult mice. In the trunk, Meis1 acts as a cofactor for genes of the Hox complex, mostly binding to Hox-Pbx target sequence on the DNA. By combining the analysis of Meis1 loss-of-function and conditional Meis1 functional rescue with ChIPseq and RNAseq approaches, we show that during the development of the optic cup, an Hox-free region, Meis1 binds instead to Hox/Pbx-independent Meis binding site, and coordinates, in a dose-dependent manner, retinal proliferation and differentiation by regulating the expression of components of the Notch signalling pathway. Meis1 also controls the activity of genes responsible for human microphthalmia and eye patterning so that in Meis1-/- embryos, the eye size is reduced and boundaries among the different eye territories are shifted or blurred. We thus propose that Meis1 is at the core of a genetic network implicated in microphthalmia, itself representing an additional candidate for syndromic cases of these ocular malformations. Overall design: Transcriptomics and Meis1 Occupancy analysis on mouse isolated optic cups and ChIP data for histone methylation marks were obtained from about 100 eyes of E10.5 CD1 embryos.
Meis1 coordinates a network of genes implicated in eye development and microphthalmia.
No sample metadata fields
View SamplesWe established and characterized a new recessive mutant mouse line kta41 with a point mutation in Scube3 at position 882. The mutant line was detected by screening for morphological abnormalities in the Munich ENU-mutagenesis program. The mutation was mapped by microsatellite markers to mouse chromosome 17, between markers D17MIT29 and D17MIT101. Candidate gene approaches failed due to the low recombination frequency and the high number of genes within the mapped interval. Whole genome sequencing approaches revealed a C to A transversion on position 882 in Scube3 that leads to a missense mutation in the protein (Asn294Lys). We did a broad phenotypic analysis of the mutant mouse line in the German Mouse Clinic (GMC), and followed up the found alterations by detailed phenotypic characterization. Scube3-kta41-/- mice show a series of phenotypic alterations, mainly in the skeleton, behavior and neurological abnormalities as well as changes in physiology, metabolism and immune status.
The First Scube3 Mutant Mouse Line with Pleiotropic Phenotypic Alterations.
Sex, Age
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