Comparison of expression profile of Ewing''s sarcoma with cell of origin, mesenchymal stem cells with the goal of identifying novel therapeutic targets. Overall design: 3 Ewing''s cell lines compared to 2 MSC cell lines
Exploring the surfaceome of Ewing sarcoma identifies a new and unique therapeutic target.
No sample metadata fields
View SamplesAfrican American men are disproportionately affected by both vitamin D deficiency and increased risk of prostate cancer.
Prostatic compensation of the vitamin D axis in African American men.
Specimen part
View SamplesStudy of HP1 Knock Down on gene expression and splicing regulation in Human HeLa cells
Histone H3 lysine 9 trimethylation and HP1γ favor inclusion of alternative exons.
Cell line
View SamplesTo study the effects of previous exposure to mechanical ventilation may modify the development of Ventilator-induced lung injury, preconditioning was induced by low-pressure ventilation for 90 minutes. After 1 week, intact (sham) and preconditioned mice were sacrificed, the lungs extracted and gene expression measured in order to identify differences responsible for the observed tolerance to ventilator-induced lung injury observed in preconditioned animals.
Exposure to mechanical ventilation promotes tolerance to ventilator-induced lung injury by Ccl3 downregulation.
Age, Specimen part
View SamplesThe whole blood was collected pre-treatment from rheumatoid arthritis patients starting the anti_TNF therapy. All patients were nave to anti_TNFs. The disease activity was measured using the DAS28 score at the pre-treatment visit1 (DAS28_v1) and 14 weeks after treatment visit3 (DAS28_v3). The response to the therapy was evaluated using the EULAR [European League Against Rheumatism] definition of the response. The objective of the data analysis was to identify gene expression coorelating with response as well as to identify genes that differentiate responders versus non-responders pre-treatment. The results of this investigation identified 8 trainscripts that predict responders vs. non-responders with 89% accuracy.
Convergent Random Forest predictor: methodology for predicting drug response from genome-scale data applied to anti-TNF response.
Specimen part, Disease, Disease stage
View SamplesThe heat shock response (HSR) is a mechanism to cope with proteotoxic stress by inducing the expression of molecular chaperones and other heat shock response genes. The HSR is evolutionarily well conserved and has been widely studied in bacteria, cell lines and lower eukaryotic model organisms. However, mechanistic insights into the HSR in higher eukaryotes, in particular in mammals, are limited. We have developed an in vivo heat shock protocol to analyze the HSR in mice and dissected heat shock factor 1 (HSF1)-dependent and -independent pathways. Whilst the induction of proteostasis-related genes was dependent on HSF1, the regulation of circadian function related genes, indicating that the circadian clock oscillators have been reset, was independent of its presence. Furthermore, we demonstrate that the in vivo HSR is impaired in mouse models of Huntington's disease but we were unable to corroborate the general repression of transcription after a heat shock found in lower eukaryotes. Overall design: RNA-Seq was performed on mRNA isolated from quadriceps femoris muscle of 24 mice. These mice were of wild type, R6/2, and Hsf1-/- genotypes. Two mice of each genotype were tested in four conditions: (1) heat shock, (2) control heat shock, (3) HSP90 inhibition (NVP-HSP990), and (4) HSP90 inhibition vehicle.
HSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.
Age, Specimen part, Treatment, Subject
View SamplesWe reported this study established a mouse model of fibrosis- and alcohol-associated AKI and identified key mechanistic pathways. Overall design: kidney mRNA profiles of Olive oil, CCl4, EtOH, and CCl4+EtOH treatment in C57BL/6 mice were generated by deep sequencing.
A mouse model of alcoholic liver fibrosis-associated acute kidney injury identifies key molecular pathways.
Sex, Specimen part, Cell line, Subject
View SamplesPhosphorylation of histone H3 at Serine 10 emerges as a mechanism increasing chromatin accessibility of the transcription factor NF-kB for a particular set of immune genes. Here we report that a bacterial pathogen uses this strategy to shape the transcriptional response of infected host cells. We identify the Shigella flexneri type III protein effector OspF as a Dual Specific Phosphatase. OspF dephosphorylates MAP kinases within the nucleus impairing histone H3 phosphorylation at Serine 10 in a gene-specific manner. Therefore, OspF reprograms the transcriptional response for inactivation of a subset of NF-kB responsive genes. This regulation leads to repression of polymorphonuclear leukocytes recruitment in infected tissues. Thus, pathogens have evolved the ability to precisely modulate host cell epigenetic information as a strategy to repress innate immunity.
An injected bacterial effector targets chromatin access for transcription factor NF-kappaB to alter transcription of host genes involved in immune responses.
No sample metadata fields
View SamplesCocoa protein content is a very interesting source for isolation of antioxidant bio-peptides, which can be used for the prevention of age-related diseases. We use microarrays to study the global genome expression of C. elegans fed with a peptide (13L) isolated from cocoa.
A cocoa peptide protects Caenorhabditis elegans from oxidative stress and β-amyloid peptide toxicity.
No sample metadata fields
View SamplesGene silencing via heterochromatin formation plays a major role in cell differentiation and maintenance of homeostasis. Here, we report the identification and characterization of a novel heterochromatinization factor in vertebrates, Bromo Adjacent Homology Domain-containing protein 1 (BAHD1). BAHD1 interacts with HP1, MBD1, HDAC5 and with several transcription factors. Through electron and immunofluorescence microscopy studies, we show that BAHD1 overexpression directs HP1 to specific nuclear sites and promotes formation of large heterochromatic domains, which lack acetyl histone H3 and are enriched in H3 trimethylated at lysine 27. Furthermore, ectopically expressed BAHD1 colocalizes with the heterochromatic X inactive chromosome. As highlighted by whole genome microarray analysis of BAHD1 knock down cells, BAHD1 represses several proliferation and survival genes and in particular, the insulin-like growth factor II gene (IGF2). BAHD1 specifically binds the CpG-rich P3 promoter of IGF2. This region contains DNA binding sequences for the transcription factor SP1, with which BAHD1 co-immunoprecipitates. Collectively, these findings provide evidence that BAHD1 acts as a silencer by recruiting proteins that coordinate heterochromatin assembly at specific sites in the genome.
Human BAHD1 promotes heterochromatic gene silencing.
Cell line
View Samples