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Eed conditional knockout in chondrocytes

ABSTRACT: Primary rib chondrocyte were isoloated from P0.5-day old wildtype and Col2-Cre:floxed EED conditional knockout mouse pups,and cultured overnight in 10%FCS containing DMEM. RNA was isolated and subjected to Affymetrix Mouse Gene ST 1.0 array. Primary rib chondrocyte were isoloated from P0.5-day old wildtype and Col2-Cre:floxed EED conditional knockout mouse pups,and cultured overnight in 10%FCS containing DMEM. RNA was isolated and subjected to Affymetrix Mouse Gene ST 1.0 array. Biological duplicate. Mice were in a mixed genetic background of C57/B6 and 129sv.

ORGANISM(S): Mus musculus

SUBMITTER: Tatsuya Kobayashi

PROVIDER: E-GEOD-66862 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Eed conditional knockout in chondrocytes

Project description:Primary rib chondrocyte were isoloated from P0.5-day old wildtype and Col2-Cre:floxed EED conditional knockout mouse pups,and cultured overnight in 10%FCS containing DMEM. RNA was isolated and subjected to Affymetrix Mouse Gene ST 1.0 array.

2015-11-01 | GSE66862 | GEO

Blockade of the neogenin-RGMb-BMP signaling hub inhibits allergen-induced airway hyperreactivtiy

Project description:Bronchial asthma is associated with type 2 immune responses induced by components of adaptive as well as innate immunity. Although innate cytokines such as IL-25 have been shown to play key roles in development of airway hyperreactivity (AHR), little is known of innate molecules that regulate IL-25-mediated airway inflammation. We found that blockade of repulsive guidance molecule b (RGMb) in an experimental murine model of asthma blocked the development of AHR, a cardinal feature of asthma, and that RGMb is expressed on F4/80+CD11b+CD11cneg macrophages (RGMb+ macrophages), which accumulated in the lungs of OVA-sensitized and challenged mice, but not in naÃ¯ve mice. Moreover, we found that a large fraction of the RGMb+ macrophages expressed the IL-25 receptor IL-17RB and produced IL-13. IL-25 was critical for the development of AHR in our model, since mice deficient in IL-17RB did not develop AHR. Finally, treatment with anti-RGMb mAb during the challenge phase of the protocol after allergen sensitization effectively prevented the development of AHR and airway inflammation, suggesting for the first time that RGMb+ cells, including RGMb+ macrophages, play critical roles in allergen-induced asthma. We used microarrays to compare the gene expression patterns in WT mice sensitized and challenged with OVA that were treated with either RGMb mAb or an isotype control. First replicate: 3 control samples (mice sensitized and challenged with saline), 3 RGMb mAb samples, 3 isotype samples; 2nd replicate: 3 control samples, 3 RGMb mAb samples, 2 isotype samples. Lung tissues were harvested at the same treatment time point in all groups.

2016-03-14 | E-GEOD-79156 | biostudies-arrayexpress

RNA profiles of total RNA and Ago2-immunoprecipitated RNA

Project description:Compared gene enrichment in Ago2-RNA immunopreciptant between wildtype and Mir140-null chondrocytes Identified Mir140 targets that are most exclusively regulated by Mir140 Biological duplicate. Total RNA and Ago2-immunoprecipitated RNA were prepared from the same primary chondrocyte culture. Chondrocytes were isolated from newborn mouse rib and cultured overnight in 10%FCS-containing medium. Total RNA and Ago2-immunoprecipitated RNA were amplified using Ovation pico, and subjected to microarray analysis (HT-mouse 430 PM). Two sets of experiments (two samples from wildtype mice for total RNA and Ago2 immunoprecipitated RNA, and two samples from Mir140-null mice for total RNA and Ago2 immunoprecipitated RNA) were performed (a total of 8 chips)

2011-06-01 | E-GEOD-27177 | biostudies-arrayexpress

Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors (SNP array)

Project description:The clinical efficacy of EGFR kinase inhibitors is limited by the development of drug resistance. The irreversible EGFR kinase inhibitor WZ4002 is effective against the most common mechanism of drug resistance mediated by the EGFR T790M mutation. Here we show that in multiple complementary models harboring EGFR T790M, resistance to WZ4002 develops through aberrant activation of ERK signaling caused by either an amplification of MAPK1 or by downregulation of negative regulators of ERK signaling. Inhibition of MEK or ERK restores sensitivity to WZ4002, and the combination of WZ4002 and a MEK inhibitor prevents the emergence of drug resistance. The WZ4002 resistant MAPK1 amplified cells also demonstrate an increase both in EGFR internalization and a decrease in sensitivity to cytotoxic chemotherapy compared to the parental counterparts. Our findings provide insights into mechanisms of drug resistance to EGFR kinase inhibitors and highlight rational combination therapies that should be evaluated in clinical trials. The EGFR mutant non-small cell lung cancer (NSCLC) cell line PC9 GR4 (delE746_A750/T790M) was exposed to increasing concentrations of WZ4002 similar to previously described methods. Individual clones from WZ4002-resistant (WZR) cells were isolated and confirmed to be drug resistant. Number of samples: 5. PC9GR4 as a control. 4 clones of WZ4002-resistant PC9GR4.

2012-10-01 | E-GEOD-37698 | biostudies-arrayexpress

Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors

Project description:This SuperSeries is composed of the following subset Series: GSE37698: Reactivation of ERK signaling causes resistance to EGFR kinase inhibitors (SNP array) GSE37699: Aberrant ERK signaling causes resistance to EGFR kinase inhibitors Refer to individual Series

2012-10-01 | E-GEOD-37700 | biostudies-arrayexpress

Integration of high-resolution methylome and transcriptome analyses to dissect epigenomic changes in childhood acute lymphoblastic leukemia

Project description:B-cell precursor acute lymphoblastic leukemia (pre-B ALL) is the most common pediatric cancer. Although the genetic origin of the disease remains unclear, epigenetic modifications including DNA methylation are suggested to contribute significantly to leukemogenesis. We assessed the DNA methylation status of 402,842 CpG-sites across the genome (Illumina 450k array) in tumor and remission samples of 46 pre-B ALL patients, thus generating the most comprehensive single CpG-site resolution pre-B ALL methylomes so far. Unsupervised hierarchical clustering of CpG-site neighborhood, protein-coding gene, or miRNA gene associated methylation levels separated the tumor cohort according to major pre-B ALL subtypes, and methylation in CpG islands, shores, and in regions around the transcription start site of protein-coding genes strongly correlated with transcript expression. Focusing on samples carrying the t(12;21)(p13;q22) translocation (ETV6-RUNX1 fusion gene) we identified subtype-specific methylation of 430 CpG-sites. Pathway analyses implied the associated genes in hematopoiesis and cancer. Further intersection with transcriptome data identified methylation to impact expression of 18 genes. In summary, our data illustrate the power of methylation profiling to classify leukemic subtypes and to identify subtype-specific methylation markers. Further, we demonstrate that integration of methylome and transcriptome alterations allows the study of downstream effects of individual genomic rearrangements in cancer. Bisulfite converted DNA of tumor (isolated on day of diagnosis) and remission (isolated after disease remission) samples derived from 46 patients of French-Canadian origin diagnosed with pre-B ALL were analyzed on the Illumina Infinium HumanMethylation 450k BeadChips.

2013-06-04 | E-GEOD-38235 | biostudies-arrayexpress

Functional analysis of ABCB5 in melanoma cells

Project description:Functional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells. 12 samples total. Replicates n=3 for the following 4 groups: A375 pSUPER-retro-puro-Vector vs. A375 pSUPER-retro-puro-ABCB5-KD; G3361 pSUPER-retro-puro-shCNTRL vs. G3361 pSUPER-retro-puro-ABCB5-KD.

2014-06-17 | E-GEOD-38290 | biostudies-arrayexpress

Affymetrix SNP array data for human prostate tumor samples

Project description:Metabolomics was used to identify metabolic fingerprints of AKT1 activation or MYC overexpression in human prostate tumors. Genomics was used to determine how many of these tumors had a genetic aberration underlying signaling activation. Copy number analysis of Affymetrix 250K SNP arrays was performed for 59 human prostate tumors and 6 normal prostate samples.

2014-10-20 | E-GEOD-62218 | biostudies-arrayexpress

Transcription profiling of mouse CD71+/Ter-119+ bone marrow erythroid progenitors from Rb-null animals and controls reveals Rb intrinsically promotes erythropoiesis by coupling cell cycle exit with mitochondrial biogenesis

Project description:Regulation of the cell cycle is intimately linked to erythroid differentiation, yet how these processes are coupled is not well understood. To gain insight into this coordinate regulation, we examined the role that the retinoblastoma protein (Rb), a central regulator of the cell cycle, plays in erythropoiesis. We found that Rb serves a cell-intrinsic role and its absence causes ineffective erythropoiesis, with a differentiation block at the transition from early to late erythroblasts. Unexpectedly, in addition to a failure to properly exit the cell cycle, mitochondrial biogenesis fails to be upregulated concomitantly, contributing to this differentiation block. The link between erythropoiesis and mitochondrial function was validated by inhibition of mitochondrial biogenesis. Erythropoiesis in the absence of Rb resembles the human myelodysplastic syndromes, where defects in cell cycle regulation and mitochondrial function frequently occur. Our work demonstrates how these seemingly disparate pathways play a role in coordinately regulating cellular differentiation. Experiment Overall Design: Microarray expression analysis from sorted CD71+/Ter-119+ bone marrow erythroid progenitors of Rb-null animals and controls. The Rb-null genotype was EpoR-GFPcre/+; Rb fl/fl and the control genotype was EpoR-GFPcre/+; Rb fl/+. We have analyzed 3 Rb-null datasets and 3 control datasets.

2008-04-07 | E-GEOD-9717 | biostudies-arrayexpress

Polycomb PRC2 antagonizes de novo DNA methylation at the maternal Gtl2-Rian-Mirg locus [Affymetrix Expression]

Project description:Wild-type mouse embryonic stem cells are compared with mutants for components of PRC2 including Ezh2-/-, Eed-/-, and Jarid2-/- cells. Gene expression microarrays were used to compare the expression for these. This experiment compares wild-type gene expression with mutants for different PRC2 components, including Ezh2-/-, Eee-/- and Jarid2-/- with two replicates for each using Affymetrix Gene Expression Arrays.

2015-07-15 | E-GEOD-59464 | biostudies-arrayexpress

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