To determine the modulation of gene expression of mouse BMDCs in the presence of living intracellular Leishmania amazonensis amastigotes at 24 hr post infection.
<i>Leishmania amazonensis</i> Subverts the Transcription Factor Landscape in Dendritic Cells to Avoid Inflammasome Activation and Stall Maturation.
Specimen part, Time
View SamplesCumulus cells are biologically distinct from other follicular cells and perform specialized roles, transmitting signals within the ovary and supporting oocyte maturation during follicular development. The bi-directional communication between the oocyte and the surrounding cumulus cells is crucial for the acquisition of oocyte competence. Using Illumina/deep-sequencing technology, we dissected the small RNAome of pooled human mature MII oocytes and cumulus cells. Overall design: Cumulus cells and MII mature oocytes small RNA profiles were generated by deep-sequencing, using Illumina 1G sequencer
MicroRNAs: new candidates for the regulation of the human cumulus-oocyte complex.
Specimen part, Subject
View SamplesAnalysis of Diffuse Large B-Cell Lymphoma (DLBCL) OCI-LY3 cell line treated with 14 different known drugs at 2 different concentrations and profiled at 6, 12 and 24 hrs after treatment.
A community computational challenge to predict the activity of pairs of compounds.
Compound, Time
View SamplesSingle O-GlcNAc modification orchestrate by O-GlcNAc Transferase (OGT) and O-GlcNAcase (OGA alias MGEA5) enzymes, affects signal transduction and gene expression by chromatin modulation. We developed Oga deleted MEF (mouse embryonic fibroblast) cells to investigate effects of O-GlcNAc modification in mice. RNA isolated from Mouse Embryonic Fibroblast cells generated from Oga Knock out (KO) Heterozygous (Het) and wild type (WT) cells and subjected to microarray analysis.
Conditional knock-out reveals a requirement for O-linked N-Acetylglucosaminase (O-GlcNAcase) in metabolic homeostasis.
Sex, Specimen part
View SamplesRhabdoid tumors (RT) are aggressive tumors characterized by genetic loss of SMARCB1 (SNF5, INI-1), a component of the SWI/SNF chromatin remodeling complex. No effective treatment is currently available. This study seeks to shed light on the SMARCB1-mediated pathogenesis of RT and to discover potential therapeutic targets. Global gene expression of 10 RT was compared with 12 cellular mesoblastic nephromas, 16 clear cell sarcomas of the kidney, and 15 Wilms tumors. 114 top genes were differentially expressed in RT (p<0.001, fold change >2 or <0.5). Among these were down-regulation of SMARCB1 and genes previously associated with SMARCB1 (ATP1B1, PTN, DOCK4, NQO1, PLOD1, PTP4A2, PTPRK). 28/114 top differentially expressed genes were involved with neural or neural crest development and were all sharply down-regulated. This was confirmed by Gene Set Enrichment Analysis (GSEA). Neural and neural crest stem cell marker proteins SOX10, ID3, CD133 and Musashi were negative by immunohistochemistry, whereas Nestin was positive. Decreased expression of CDKN1A, CDKN1B, CDKN1C, CDKN2A, and CCND1 was identified, while MYC-C was upregulated. GSEA of independent gene sets associated with bivalent histone modification and polycomb group targets in embryonic stem cells demonstrated significant negative enrichment in RT. Several differentially expressed genes were associated with tumor suppression, invasion and metastasis, including SPP1 (osteopontin), COL18A1 (endostatin), PTPRK, and DOCK4. We conclude that RTs arise within early progenitor cells during a critical developmental window in which loss of SMARCB1 directly results in repression of neural development, loss of cyclin dependent kinase inhibition, and trithorax/polycomb dysregulation.
Rhabdoid tumor: gene expression clues to pathogenesis and potential therapeutic targets.
No sample metadata fields
View SamplesThis study identifies miR-198 as a potential inhibitor of keratinocyte migration in skin
'See-saw' expression of microRNA-198 and FSTL1 from a single transcript in wound healing.
Specimen part, Time
View SamplesProstate cancer is dependent on androgen receptor (AR) signaling at all stages of the disease and cyclin D1 has been shown to negatively modulate the expression of the AR-dependent gene prostate specific antigen (KLK3/PSA).
Cyclin D1 is a selective modifier of androgen-dependent signaling and androgen receptor function.
Cell line, Treatment
View SamplesBAF57, a component of the SWI/SNF chromatin remodeling complex conglomerate,modulates androgen receptor activity to promote prostate cancer. However the molecular consequences of tumor associated BAF57 elevation have remianed undefined in advanced disease such as castration resistant prostate cancer and/or metastasis
Aberrant BAF57 signaling facilitates prometastatic phenotypes.
Specimen part, Treatment
View SamplesThe study of the mechanisms leading to cardiac hypertrophy is essential to better understand cardiac development and regeneration. Pathological conditions such as ischemia or pressure overload can induce a release of extracellular nucleotides within the heart. We recently investigated the potential role of nucleotide P2Y receptors in cardiac development. We showed that adult P2Y4-null mice displayed microcardia resulting from defective cardiac angiogenesis. Here we show that loss of another P2Y subtype called P2Y6, a UDP receptor, was associated with a macrocardia phenotype and amplified pathological cardiac hypertrophy. Cardiomyocyte proliferation and size were increased in vivo in hearts of P2Y6-null neonates, resulting in enhanced post-natal heart growth. We then observed that loss of P2Y6 receptor enhanced pathological cardiac hypertrophy induced after isoproterenol injection. We identified an inhibitory effect of UDP on in vitro isoproterenol-induced cardiomyocyte hyperplasia and hypertrophy. The present study identifies mouse P2Y6 receptor as a regulator of cardiac development and cardiomyocyte function. P2Y6 receptor could constitute a therapeutic target to regulate cardiac hypertrophy. Overall design: WT and P2Y6 KO mice aged between 8 and 12 weeks were intraperitoneally injected with 50 mg/kg/day isoproterenol or saline solution, daily during 7 days, then hearts were harvested and weighted. Ventricles were then stored for RNA extraction.
Loss of Mouse P2Y6 Nucleotide Receptor Is Associated with Physiological Macrocardia and Amplified Pathological Cardiac Hypertrophy.
Specimen part, Treatment, Subject
View SamplesTo understand the underlying cause and mechanisms of embryonic lethality observed in combined loss of E2f7 and E2f8, we compared global gene expression profiles of wild type, germline deleted and sox2-Cre/Cyp19-Cre deleted embryos and placentas.
Atypical E2F repressors and activators coordinate placental development.
Specimen part
View Samples