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SRP067017
Homo sapiens
4 Downloadable Samples
Illumina HiSeq 2000
Description
We evaluated the transcriptome changes induced by infection of Hela 229 cells with Shigella flexneri. The sample set consists of a control (mock), total population of infected sample and infected sample sorted into Shigella positive and Shigella negative population. Overall design: Transcriptmic profiles of HeLa cells infected with Shigella were generated by high throughput sequencing using Illumina HiSeq2000.
Publication Title
Analysis of host microRNA function uncovers a role for miR-29b-2-5p in Shigella capture by filopodia.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 2 Downloadable Samples
- IlluminaHiSeq2000
Description
To have a global picture of the targets of the mir-29b-2-5p, we assessed transcriptome changes, by deep-sequencing, of HeLa cells transfected with this miRNA or a control miRNA (cel-miR-231). Overall design: Transcriptmic profiles of HeLa cells treated miR-29b-2-5p and control-miR were generated by deep sequencing, using Illumina HiSeq2000.
Publication Title
Analysis of host microRNA function uncovers a role for miR-29b-2-5p in Shigella capture by filopodia.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 117 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
Muscle biopsies taken from vastus lateralis muscle of 15 men and 15 women after 3 days of standardized diet and activity to examine effects of sex and age
Publication Title
Sex-related differences in gene expression in human skeletal muscle.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
RNA from 5 mice with postdevelopmental knockout of myostatin and 5 mice with normal myostatin expression was analyzed with comprehensive oligonucleotide microarrays. Myostatin depletion affected the expression of several hundred genes at nominal P < 0.01, but fewer than a hundred effects were statistically significant according to a more stringent criterion (false discovery rate < 5%). Most of the effects were less than 1.5-fold in magnitude. In contrast to previously-reported effects of constitutive myostatin knockout, postdevelopmental knockout did not downregulate expression of genes encoding slow isoforms of contractile proteins or genes encoding proteins involved in energy metabolism. Several collagen genes were expressed at lower levels in the myostatin-deficient muscles, and this led to reduced tissue collagen levels as reflected by hydroxyproline content. Myostatin knockout tended to down-regulate the expression of sets of genes with promoter motifs for Smad3, Smad4, myogenin, NF-B, serum response factor, and numerous other transcription factors. Main conclusions: in mature muscle, myostatin is a key transcriptional regulator of collagen genes, but not genes encoding contractile proteins or genes encoding proteins involved in energy metabolism.
Publication Title
Skeletal muscle gene expression after myostatin knockout in mature mice.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 196 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Muscle biopsies taken from vastus lateralis muscle of 30 normal subjects and 19 FSHD subjects (see PubMed ID 17151338)
Publication Title
Expression profile of FSHD supports a link between retinal vasculopathy and muscular dystrophy.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
The gene expression pathways leading to muscle pathology in facioscapulohumeral dystrophy (FSHD) remain to be elucidated. This muscular dystrophy is caused by a contraction of an array of tandem 3.3-kb repeats (D4Z4) at 4q35.2. We compared expression of control and FSHD myoblasts and myotubes (three preparations each) on exon microarrays (Affymetrix Human Exon 1.0 ST) and validated FSHD-specific differences for representative genes by qRT-PCR on additional myoblast cell strains. The FSHD and control myoblasts used for these experiments were shown to grow and differentiate into myotubes equally efficiently as control myoblasts. There were no significant FSHD-control differences in RNA levels for MYOD1 and MYOG at the myoblast and myotube stages and for MYF5 and MYF6 at the myoblast stage. In contrast, 295 other genes were dysregulated at least 2-fold in FSHD vs. control myoblasts (p <0.01, adjusted for multiple comparisons).
Publication Title
Gene expression during normal and FSHD myogenesis.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 36 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Facioscapulohumeral dystrophy (FSHD) is one of the most common inherited muscular dystrophies. The causative gene remains controversial and the mechanism of pathophysiology unknown. Here we identify genes associated with germline and early stem cell development as targets of the DUX4 transcription factor, a leading candidate gene for FSHD. The genes regulated by DUX4 are reliably detected in FSHD muscle but not in controls, providing direct support for the model that misexpression of DUX4 is a causal factor for FSHD. Additionally, we show that DUX4 binds and activates LTR elements from a class of MaLR endogenous primate retrotransposons and suppresses the innate immune response to viral infection, at least in part through the activation of DEFB103, a human defensin that can inhibit muscle differentiation. These findings suggest specific mechanisms of FSHD pathology and identify candidate biomarkers for disease diagnosis and progression.
Publication Title
DUX4 activates germline genes, retroelements, and immune mediators: implications for facioscapulohumeral dystrophy.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 32 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
Clinical symptoms of dengue virus (DENV) infection, the most prevalent arthropod-borne viral disease, range from classical mild dengue fever to severe, life-threatening dengue shock syndrome. However, most DENV infections cause few or no symptoms. Asymptomatic DENV-infected patients provide a unique opportunity to decipher the host immune responses leading to virus elimination without negative impact on an individuals health. We used an integrated approach of transcriptional profiling and immunological analysis to compare a Cambodian population of strictly asymptomatic viremic individuals with clinical dengue patients. Whereas inflammatory pathways and innate immune response pathways were similar between asymptomatic individuals and clinical dengue patients, expression of proteins related to antigen presentation and subsequent T and B cell activation pathways were differentially regulated, independent of viral load and previous DENV infection history. Feedback mechanisms controlled the immune response in asymptomatic viremic individuals, as demonstrated by increased activation of T cell apoptosis-related pathways and FcRIIB signaling associated with decreased anti-DENV specific antibody concentrations. Taken together, our data illustrate that symptom-free DENV infection in children is associated with determined by increased activation of the adaptive immune compartment and proper control mechanisms, leading to elimination of viral infection without excessive immune activation, with implications for novel vaccine development strategies
Publication Title
Increased adaptive immune responses and proper feedback regulation protect against clinical dengue.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Dendritic cells (DCs) are pivotal for both recognition of antigens and control of an array of immune responses by recognizing microbes through distinct pattern recognition receptors (PRRs). The first microbial component to be studied in detail and known to cause septic shock is endotoxin (LPS). DCs recognize LPS via Toll-like receptor TLR-47. LPS causes many changes in the DCs, but the elicitation of cytokine production is perhaps the one with clear biologic relevance.
Publication Title
Targeting of microRNA-142-3p in dendritic cells regulates endotoxin-induced mortality.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Rattus norvegicus
- 94 Downloadable Samples
- Affymetrix Rat Gene 2.1 ST Array (ragene21st)
Description
Predicting liver injury after exposure to toxic industrial chemicals is complicated by the large number of potential environmental contaminants, mixtures, and exposure dose and route scenarios. Identifying indicators of end organ injury can complement exposure-based assays and improve predictive power. A multiplexed approach was used to experimentally evaluate a panel of 67 genes predicted to be fibrogenic by computationally mining DrugMatrix, a publicly available repository of gene microarray data. Five-day oral gavage studies in male Sprague-Dawley rats dosed with varying concentrations of three fibrogenic compounds (allyl alcohol, carbon tetrachloride, and 4,4-methylenedianiline) and two non-fibrogenic compounds (bromobenzene and dexamethasone) were conducted. Fibrosis was definitively diagnosed by histopathology. Transcriptomics data matched the predictions made using the DrugMatrix data with greater than 90% accuracy. Microarray data were verified using a 67-plex panel Bioplex assay, confirming that the 67-plex panel constituted a biomolecular signature of hepatic fibrosis (Figure). Necrosis and inflammatory infiltration were comorbid with fibrosis. Interaction analysis identified 24 genes specific for the fibrosis phenotype. The protein product of the gene most strongly correlated with the fibrosis phenotype (Pcolce) was dose-dependently elevated in plasma from animals administered fibrogenic chemicals (p<0.05). PCOLCE is a novel biomarker candidate of fibrotic injury. These results support the development of gene panels for liver injury and may suggest bridging biomarkers for molecular mediators linked to histopathology.
Publication Title
Gene Expression Patterns Associated With Histopathology in Toxic Liver Fibrosis.
Sample Metadata Fields
Sex, Specimen part
View Samples