Trascriptome analysis of osteosarcoma samples were performed Overall design: Tumor samples were obtained from a previously published Sleeping Beauty forward genetic screen, cell lines were derived from previous primary tumors and sequenced using Illumina HiSeq 2000
Comparative Transcriptome Analysis Quantifies Immune Cell Transcript Levels, Metastatic Progression, and Survival in Osteosarcoma.
Specimen part, Cell line, Subject
View SamplesWe report RNA sequencing data from tenocytes treated with IGF1. Tenocytes were obtained from the tail tendons of adult C57Bl/6 mice via collagenase digestion. Tenocytes were grown to 60% confluence, and then treated with 100ng/mL of recombinant IGF1 for a period of 0, 1, 2, 6, or 24 hours. Experiments were conducted in quadruplicate. RNA was isolated and prepared for RNA sequencing. Overall design: Differential expression of mRNAs were evaluated from tenocytes isolated from tail tendons of adult wild type C57Bl/6 mice that were treated with recombinant IGF1 for 0, 1, 2, 6, and 24 hours.
Insulin-like growth factor 1 signaling in tenocytes is required for adult tendon growth.
Specimen part, Cell line, Subject
View SamplesDmrt1 (doublesex and mab-3 related transcription factor 1) is a conserved transcriptional regulator of male differentiation required for testicular development in vertebrates. This study examines the result of conditional removal of Dmrt1 from Sertoli cells in P28 testis tissue.
DMRT1 prevents female reprogramming in the postnatal mammalian testis.
Sex, Specimen part
View SamplesBackground: Bone marrow-derived multipotent progenitor cell (MPC) transplantation leads to short term functional and bioenergetic improvement in a porcine model of postinfarction Left Ventricular (LV) remodeling despite a low engraftment rate. However, the long term outcome after MPC transplantation is unknown.
Long-term functional improvement and gene expression changes after bone marrow-derived multipotent progenitor cell transplantation in myocardial infarction.
Sex, Specimen part, Treatment
View SamplesPlatelet-derived growth factor receptor (PDGFR) signaling plays an important role in the embryonic formation of many different tissues. There is a family of PDGF isoforms which signal through the PDGF receptors (PDGFR) and (PDGFR). PDGF regulates many key cellular processes of mesenchymal cell function including proliferation, differentiation, migration and extracellular matrix (ECM) synthesis. While PDGF has been used to enhance flexor tendon healingin vivo, its role in postnatal tendon growth has remained largely unexplored. To determine the importance of PDGFR signaling in postnatal tendon growth, we performed pharmacological blockade of PDGFR and PDGFR, and then induced tendon growth via mechanical overload using the hindlimb synergist ablation model. Our hypothesis was that inhibition of PDGFR signaling will restrict normal growth of tendon tissue in response to mechanical loading.
Postnatal tendon growth and remodeling require platelet-derived growth factor receptor signaling.
Sex, Treatment
View SamplesTherapies targeting the type I insulin-like growth factor receptor (IGF-1R) have not been developed with predictive biomarkers to identify tumors with receptor activation. We have previously shown that the insulin receptor substrate (IRS) adaptor proteins are necessary for linking IGF1R to downstream signaling pathways and the malignant phenotype in breast cancer cells. The purpose of this study was to identify gene expression profiles downstream of IGF1R and its two adaptor proteins. IRS-null breast cancer cells (T47D-YA) were engineered to express IRS-1 or IRS-2 alone and their ability to mediate IGF ligand-induced proliferation, motility, and gene expression determined. Global gene expression signatures reflecting IRS adaptor specific and primary vs. secondary ligand response were derived (Early IRS-1, Late IRS-1, Early IRS-2 and Late IRS-2) and functional pathway analysis examined. IRS isoforms mediated distinct gene expression profiles, functional pathways, and breast cancer subtype association. For example, IRS-1/2-induced TGFb2 expression and blockade of TGFb2 abrogated IGF-induced cell migration. In addition, the prognostic value of IRS proteins was significant in the luminal B breast tumor subtype. Univariate and multivariate analyses confirmed that IRS adaptor signatures correlated with poor outcome as measured by recurrence-free and overall survival. Thus, IRS adaptor protein expression is required for IGF ligand responses in breast cancer cells. IRS-specific gene signatures represent accurate surrogates of IGF activity and could predict response to anti-IGF therapy in breast cancer.
Insulin Receptor Substrate Adaptor Proteins Mediate Prognostic Gene Expression Profiles in Breast Cancer.
Cell line
View SamplesDmrt1 (doublesex and mab-3 related transcription factor 1) is a conserved transcriptional regulator of male differentiation required for testicular development in vertebrates. In mice of the 129Sv strain, loss of Dmrt1 causes a high incidence of teratomas. Mutant 129Sv germ cells undergo apparently normal differentiation up to embryonic day 13.5 (E13.5), but some cells fail to arrest mitosis and ectopically express pluripotency markers. Expression analysis and chromatin immunoprecipitation identified DMRT1 target genes whose misexpression may underly teratoma formation.
The DM domain protein DMRT1 is a dose-sensitive regulator of fetal germ cell proliferation and pluripotency.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.
Specimen part, Cell line, Time
View SamplesMutant RAS oncoproteins activate signaling molecules that drive oncogenesis in multiple human tumors including acute myelogenous leukemia (AML). However, the specific function of these pathways in AML is unclear. To elucidate the downstream functions of activated NRAS in AML, we employed a murine model of AML harboring Mll-AF9 and NRASG12V. We found that NRASG12V enforced leukemia self-renewal gene expression signatures and was required to maintain an MLL-AF9 and MYB-dependent gene expression program. In a multiplexed analysis of RAS-dependent signaling intermediates, the leukemia stem cell compartment was preferentially sensitive to RAS withdrawal. Use of RAS-pathway inhibitors showed that NRASG12V maintained leukemia self-renewal through mTOR and MEK pathway activation, implicating these pathways as potential targets for cancer stem cell-specific therapies. Overall design: Primary leukemia cells harvested from spleens were sorted into immunophenotypic subpopulations (Mac-1High, Mac-1LowKit–Sca-1–, Mac-1LowKit+Sca-1–, and Mac-1LowKit+Sca-1+). RNA was extracted from this subpopulations of cells and submitted for RNA sequencing.
NRASG12V oncogene facilitates self-renewal in a murine model of acute myelogenous leukemia.
No sample metadata fields
View Samples