Bisphenol-A is a widespread endocrine disruptor chemical. In utero or perinatal exposure to bisphenol-A (BPA), leads to impaired glucose metabolism during adulthood. To investigate the consequences of the exposure to bisphenol-A during development in pancreatic beta-cell growth
Maternal Exposure to Bisphenol-A During Pregnancy Increases Pancreatic β-Cell Growth During Early Life in Male Mice Offspring.
Sex, Specimen part
View SamplesPurpose: Osteoblast cells mature from a mesenchymal stem cell pool to become cells capable of forming bone matrix and mineralizing this matrix. The goal of this study was to characterize temporal changes in the transcriptome across osteoblast maturation, starting with committed mesenchymal stem cell/ early pre-osteoblast stage through to mature osteoblasts capable of matrix mineralization. Methods: Enriched populations of pre-osteoblast like cells were obtained from neonatal calvaria from C57BL/6J mice expressing CFP under the control of the Col3.6 promoter. These cells were placed into culture for 4 days, removed from culture and subjected FACS sorting based on the presence/absence of CFP expression. Cells expressing CFP were returned to culture, subjected to an osteoblast differentiation cocktail and RNA was collected at 2, 4, 6, 8, 10, 12, 14, 16 and 18 days post differentiation. Methods II: mRNA profiles for each time point were generated by next generation RNA sequencing, using an Illumina HiSeq 2000. Three technical replicates per samples were sequenced. The alignments for abundance estimation of transcripts was conducted using Bowtie version 0.12.9, using the NCBIm37 reference genome. Expression level per gene was calculated using RSEM version 1.2.0 with the parameters of --fragment-length-mean 280 and --fragment-length-sd 50, and the expression level for each sample was normalized relative to the per sample upper quartile. Overall design: Gene expression in calvarial osteoblasts from neonatal C57BL/6J-Col3.6 CFP mice at 9 time points post differentiation
Identification of 153 new loci associated with heel bone mineral density and functional involvement of GPC6 in osteoporosis.
No sample metadata fields
View SamplesMetazoan development depends on accurate execution of differentiation programs that allow pluripotent stem cells to adopt specific fates. Differentiation is brought about by global changes to chromatin architecture and transcriptional networks, yet whether other regulatory events support cell fate determination is less well understood. Using a human embryonic stem cell model, we identified the vertebrate-specific ubiquitin ligase Cul3KBTBD8 as an essential regulator of neural crest cell formation. Cul3KBTBD8 monoubiquitylates NOLC1 and its paralog TCOF1, whose mutation underlies the developmental disease Treacher Collins Syndrome that is characterized by a loss of cranial neural crest cells. Ubiquitylation of NOLC1 and TCOF1 drives formation of a platform that connects RNA polymerase I with ribosome modification enzymes, thereby altering the translational program of differentiating cells to support the generation of neural crest cells. We conclude that the dynamic regulation of ribosome function is an important feature of cell fate determination.
Cell-fate determination by ubiquitin-dependent regulation of translation.
Cell line
View SamplesStatins reduce cardiovascular disease risk by lowering plasma low density lipoprotein (LDL)-cholesterol. To identify novel pathways that modulate statin response, we assessed the influence of simvastatin exposure on expression quantitative trait locus (eQTL) associations across the genome in 480 lymphoblastoid cell lines (LCLs). Cell lines were derived blood samples collected ant entry visit from participants in the Cholesterol and Pharmacogenomics (CAP) trial, who underwent a 6 week 40mg/day simvastatin trial. We identified 4590 cis-eQTLS that were independent of treatment status (FDR=1%) and six cis-eQTLS for which there was evidence of an interaction with treatment (FDR=20%). Genotypes and Phenotypes derived from these indivudals are available through dbGaP (Accession Number). eQTL results are available at: http://eqtl.uchicago.edu/cgi=bin/gbrowse/eqtl/
HNRNPA1 regulates HMGCR alternative splicing and modulates cellular cholesterol metabolism.
Sex, Subject
View SamplesWe performed affymetrix gene expression profiling on mammary tumors from eight well-characterized genetically engineered Mouse (GEM) models of human breast cancer.
Integrated miRNA and mRNA expression profiling of mouse mammary tumor models identifies miRNA signatures associated with mammary tumor lineage.
Specimen part
View SamplesMicroRNAs (miRNAs) are a class of small RNA molecules that regulate expression of specific mRNA targets. They can be released from cells, often encapsulated within extracellular vesicles (EVs), and therefore have the potential to mediate intercellular communication. It has been suggested that certain miRNAs may be selectively exported, although the mechanism has yet to be identified. Manipulation of the miRNA content of EVs will be important for future therapeutic applications. We therefore wished to assess which endogenous miRNAs are enriched in EVs and how effectively an overexpressed miRNA would be exported. Small RNA libraries from HEK293T cells and vesicles before or after transfection with a vector for miR-146 overexpression were analysed by deep sequencing. A subset of miRNAs was found to be enriched in EVs. The global expression data provided by deep sequencing confirms that specific miRNAs are enriched in EVs released by HEK293T cells. Overall design: Cells were transfected with a plasmid to direct overexpression of miR-146a. Extracellular vesicles were isolated by ultracentrifugation from untreated and transfected cells. RNA was isolated from one sample each of untreated and transfected cells and vesicles.Small RNA libraries were prepared for sequencing.
Selective extracellular vesicle-mediated export of an overlapping set of microRNAs from multiple cell types.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Suboptimal evolutionary novel environments promote singular altered gravity responses of transcriptome during Drosophila metamorphosis.
Sex, Age
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer.
Specimen part, Disease, Disease stage
View SamplesGenome-wide transcriptional profiling showed that reducing gravity levels in the International Space Station (ISS) causes important alterations in Drosophila gene expression intimately linked to imposed spaceflight-related environmental constrains during Drosophila metamorphosis. However, simulation experiments on ground testing space-related environmental constraints, show differential responses. Curiously, although particular genes are not common in the different experiments, the same GO groups including a large multigene family related with behavior, stress response and organogenesis are over represented in them. A global and integrative analysis using the gene expression dynamics inspector (GEDI) self-organizing maps, reveals different degrees in the responses of the transcriptome when using different environmental conditions or microgravity/hypergravity simulation devices
Suboptimal evolutionary novel environments promote singular altered gravity responses of transcriptome during Drosophila metamorphosis.
No sample metadata fields
View SamplesWe used gene expression profiling of human DCIS and IBC to discover uniquely expressed genes that may also regulate progression.
Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer.
Specimen part, Disease, Disease stage
View Samples