It has long been appreciated that striped pair-rule transcription factor expression is necessary for convergent extension in the early Drosophila embryo, although the mechanisms that link these transcriptional regulators to planar polarity in this tissue have long been elusive. The goal of this study was to determine the transcriptional tragets of the pair-rule transcription factors Eve and Runt in Drosophila blastoderm embryos. We compared the transcriptional profiles of late blastoderm embryos injected with either water or dsRNAs against both eve and runt to identify differentially expressed genes that may directly contribute to the establishment of planar polarity during Drosophila convergent extension. Overall design: Comparing the mRNA profiles from late blastoderm Drosophila embryos injected with either water (Water) or eve+runt dsRNAs (Eve), in triplicate, using Illumina HiSeq.
A positional Toll receptor code directs convergent extension in Drosophila.
Subject
View SamplesIn this study, we jointly profiled mRNA and miRNA expression to determine the role of miRNAs in AD, and whether the levels of miRNAs are related to those of target mRNAs. We found a bias towards positive correlation between levels of miRNAs and those of their targets.
Joint genome-wide profiling of miRNA and mRNA expression in Alzheimer's disease cortex reveals altered miRNA regulation.
Sex, Age, Specimen part, Disease
View SamplesIn the present study, we analyze the effect of knocking down LSG1 and KRas(V12D) overexpression in MRC5 cells in the transcriptome using Ampliseq RNA sequencig. We observed that shLSG1 induced a potent senescence response that is characterized by the activation of ER-Stress and cholesterol biosynthetic pathway Overall design: MRC5 were transfected with siRNA to knockdown the small GTPase LSG1. Total mRNA was extracted and expression profiles were analyzed.
Inhibition of the 60S ribosome biogenesis GTPase LSG1 causes endoplasmic reticular disruption and cellular senescence.
Specimen part, Cell line, Subject
View SamplesA transcriptomic meta-analysis of over 400 microarrays was undertaken to compare LPC lines against datasets of; muscle and embryonic stem cell lines, embryonic and developed liver (DL), and HCC. Uploaded here, is the array data from seven of the ten LPC lines used. These seven were prepared in our laboratory. The remaining LPC arrays and arrays from other tissues/cells were obtained from the GEO.
A Transcriptomic Signature of Mouse Liver Progenitor Cells.
Sex, Specimen part
View SamplesLong-term pharmacological glucocorticoid therapy causes atrophy and hypofunction of the adrenal cortex. Following glucocorticoids withdrawal, a functional and anatomic regeneration take place, whose cellular and molecular mechanisms are poorly understood
Sonic Hedgehog and WNT Signaling Promote Adrenal Gland Regeneration in Male Mice.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Protein kinase c-β-dependent activation of NF-κB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia B cells in vivo.
Specimen part, Cell line
View SamplesTumor cell survival critically depends on heterotypic communication with benign cells in the microenvironment. Here we describe a novel survival signaling pathway activated in stromal cells by contact to B-cells from chronic lymphocytic leukemia (CLL) patients. The expression of PKC-II and the subsequent activation of NF-B in bone marrow stromal cells is a prerequisite to support the survival of malignant B-cells. PKC- knockout mice are insusceptible to CLL-transplantations, underscoring the in vivo significance of the PKC-II- NF-B signaling pathway in the tumor microenvironment. Upregulated stromal PKC-II in biopsies from CLL, breast- and pancreatic- cancer patients suggest that this pathway may commonly be activated in a variety of malignancies.
Protein kinase c-β-dependent activation of NF-κB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia B cells in vivo.
Specimen part
View SamplesTumor cell survival critically depends on heterotypic communication with benign cells in the microenvironment. Here we describe a novel survival signaling pathway activated in stromal cells by contact to B-cells from chronic lymphocytic leukemia (CLL) patients. The expression of PKC-II and the subsequent activation of NF-B in bone marrow stromal cells is a prerequisite to support the survival of malignant B-cells. PKC- knockout mice are insusceptible to CLL-transplantations, underscoring the in vivo significance of the PKC-II- NF-B signaling pathway in the tumor microenvironment. Upregulated stromal PKC-II in biopsies from CLL, breast- and pancreatic- cancer patients suggest that this pathway may commonly be activated in a variety of malignancies.
Protein kinase c-β-dependent activation of NF-κB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia B cells in vivo.
Specimen part, Cell line
View SamplesAlveolar rhabdomyosarcomas (ARMS) are aggressive soft-tissue sarcomas affecting children and young adults. Most ARMS tumors express the PAX3-FKHR or PAX7-FKHR (PAX-FKHR) fusion genes resulting from the t(2;13) or t(1;13) chromosomal translocations, respectively. However, up to 25% of ARMS tumors are fusion negative, making it unclear whether ARMS represent a single disease or multiple clinical and biological entities with a common phenotype. To test to what extent PAX-FKHR determine class and behavior of ARMS, we used oligonucleotide microarray expression profiling on 139 primary rhabdomyosarcoma tumors and an in vitro model. We found that ARMS tumors expressing either PAX-FKHR gene share a common expression profile distinct from fusion-negative ARMS and from the other rhabdomyosarcoma variants. We also observed that PAX-FKHR expression above a minimum level is necessary for the detection of this expression profile. Using an ectopic PAX3-FKHR and PAX7-FKHR expression model, we identified an expression signature regulated by PAX-FKHR that is specific to PAX-FKHR-positive ARMS tumors. Data mining for functional annotations of signature genes suggested a role for PAX-FKHR in regulating ARMS proliferation and differentiation. Cox regression modeling identified a subset of genes within the PAX-FKHR expression signature that segregated ARMS patients into three risk groups with 5-year overall survival estimates of 7%, 48%, and 93%. These prognostic classes were independent of conventional clinical risk factors. Our results show that PAX-FKHR dictate a specific expression signature that helps define the molecular phenotype of PAX-FKHR-positive ARMS tumors and, because it is linked with disease outcome in ARMS patients, determine tumor behavior.
Identification of a PAX-FKHR gene expression signature that defines molecular classes and determines the prognosis of alveolar rhabdomyosarcomas.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesIn order to investigate genes regulated by Wnt/Beta-catenin-signaling in immortalized mouse adrenocortical cells, we treated a pair of ATCL7 cell cultures, one with BIO, a small molecule mimicking Wnt/Beta-catenin-signaling, the other with a control treatment. We repeated this 3 additional times resulting in 4 pairs of samples. The Wnt/beta-catenin pathway is not basally active in ATCL7 cells, nor do these cells appear to contain any mutations in the Wnt/Beta-catenin pathway. ATCL7 cells were grown under standard conditions at 37C in a humidified incubator containing 5% CO2. 250,000 ATCL7 cells per sample were treated with 0.5uM BIO (6-Bromoindirubin-3'-oxime) or 0.01% DMSO (v/v) for 24 hours, in DMEM:F12 growth media containing 100U/mL pencillin/streptomycin, 1X insulin-transferrin-selenium-X, 0.025% fetal bovine serum and 0.025% horse serum. Cells were harvested and RNA was extracted using an RNeasy Plus Mini Kit (Qiagen). Biotinylated cDNA were prepared according to the Ambion WT kit protocol from 250 ng total RNA (GeneAtlas WT Expression Kit User Manual P/N 702935 Rev. 3). We assayed the targets with Affymetrix Mouse Gene ST 1.1 strip arrays. We modeled the data using paired T-tests for each probe-set. We also supply a supplementary file holding the data and some statistical analysis, as well as probe-set annotation that we used at that time (users may wish to obtain new annotation though). We analyzed only 28944 probe-sets with category "main", "---", and "flmrna->unmapped" according to Affymetrix annotation.
Wnt signaling inhibits adrenal steroidogenesis by cell-autonomous and non-cell-autonomous mechanisms.
Sex, Specimen part, Cell line, Treatment
View Samples