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SRP001010
Caenorhabditis elegans
11 Downloadable Samples
Illumina Genome Analyzer
Description
While the genome sequence of many animals is now complete, their transcriptomes are less well characterised. Both genome-scale tiling arrays and massively parallel sequencing now allow transcriptomes to be mapped at unprecedented depth. We used both technologies to map the C. elegans transcriptome across development. This unbiased overview can serve as a framework for assessing transcriptome changes in a mutant animal and we compared the wild-type data with that of animals that have lost the nonsense-mediated decay (NMD) pathway. Results We find that while the great majority of detectable transcripts map to known gene structures, over 5% of transcribed regions are novel, falling outside current gene annotations. We show that at least 40% of these are novel exons. We also used both technologies to assess isoform complexity and estimate that at least 17% of genes change their major isoform across development. Having mapped the wild-type transcriptome, we examined how this is perturbed in animals lacking nonsense -mediated decay (NMD). NMD prevents expression of prematurely truncated proteins by degrading transcripts containing premature termination codons (PTCs). We find that ~20% of all genes produce transcripts that appear to be targets for NMD. While most of these arise from splicing errors, NMD targets are also enriched for transcripts that contain short open reading frames upstream of the predicted translational start (uORFs). We find an intriguing relationship between the strength of Kozak consensus surrounding the true start codon and the degree to which these uORF containing transcripts are targeted by NMD, suggesting that translational efficiency may be coupled to transcript turnover via the NMD pathway for many transcripts. Conclusions We have generated a high-resolution map of the C. elegans transcriptome and have used it to identify transcripts that are endogenous targets of the NMD machinery. We find that these targets arise principally through splicing errors and suggest that splicing and NMD are highly interlinked processes.
Publication Title
High resolution transcriptome maps for wild-type and nonsense-mediated decay-defective Caenorhabditis elegans.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We investigated the transcriptional effects of p63 binding by analyzing ME180 cells depleted for all p63 isoforms via expression of a small hairpin RNA (shRNA) targeting the p63 oligomerization domain.
Publication Title
Relationships between p63 binding, DNA sequence, transcription activity, and biological function in human cells.
Sample Metadata Fields
Age
View Samples- Drosophila melanogaster
- 8 Downloadable Samples
- Illumina Genome Analyzer
Description
Deep Sequencing of Kc167 mRNA. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Overall design: Seq of Poly-A+ RNA from D. melanogaster Kc167
Publication Title
The transcriptional diversity of 25 Drosophila cell lines.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 29 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Multiple sclerosis (MS) is a neurodegenerative disease with a presumed autoimmune component. Expression profiling in immune cells can therefore be used in order to identify genes and pathways involved in MS pathogenesis.
Publication Title
Systematic review of genome-wide expression studies in multiple sclerosis.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Bos taurus
- 1 Downloadable Sample
- Illumina HiSeq 2000
Description
Sequencing of a pool of 9 bulls of varying conception rate (CR) scores from -2.9 to 3.5.
Publication Title
Cryopreserved bovine spermatozoal transcript profile as revealed by high-throughput ribonucleic acid sequencing.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 57 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Illumina HumanMethylation450 BeadChip (HumanMethylation450_15017482)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Subcutaneous adipose tissue gene expression and DNA methylation respond to both short- and long-term weight loss.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Homo sapiens
- 57 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
To understand the temporal changes occurring in adipose tissue gene expression during a one-year weightloss intervention, adipose tissue biopsies were collected from 19 healthy obese individuals at three time points.
Publication Title
Subcutaneous adipose tissue gene expression and DNA methylation respond to both short- and long-term weight loss.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Rheumatoid arthritis (RA) leads to progressive destruction of articular structures. Despite recent progress in controlling inflammation and pain, little cartilage repair has yet been observed. This in vitro study aims to determine the role of chondrocytes in RA-related cartilage destruction and antirheumatic drug-related regenerative processes. Human chondrocytes were three-dimensionally cultured in alginate beads. To determine the RA-induced gene expression pattern, human chondrocytes were stimulated with supernatant of RA synovial fibroblasts (RASF) and normal donor synovial fibroblasts (NDSF), respectively. To examine antirheumatic drug response signatures, human chondrocytes were stimulated with supernatant of RASF that have been treated with disease-modifying antirheumatic drugs (DMARD; azathioprine, sodium aurothiomalate, chloroquine phosphate, methotrexate), non-steroidal anti-inflammatory drugs (NSAID; piroxicam, diclofenac) or steroidal anti-inflammatory drugs (SAID; methylprednisolone, prednisolone). Genome-wide expression profiling with oligonucleotide microarrays was used to determine differentially expressed genes. Real-time RT-PCR and ELISA were performed for validation of microarray data. Following antirheumatic treatment, microarray analysis disclosed a reverted expression of 94 RA-induced chondrocyte genes involved in inflammation/NF-B signalling, cytokine/chemokine activity, immune response, proliferation/differentiation and matrix remodelling. Hierarchical clustering analysis showed that treatment of RASF with the DMARD azathioprine, gold sodium thiomalate and methotrexate resulted in chondrocyte gene expression signatures that were closely related to the healthy pattern. Treatment with the SAID methylprednisolone and prednisolone strongly reverted the RA-related chondrocyte gene expression, in particular the expression of genes involved in inflammation/NF-B and cytokine/chemokine activity. The NSAID piroxicam and diclofenac and the DMARD chloroquine phosphate had only moderate to marginal effects. Pathway analysis determined major mechanisms of drug action, for example pathways of cytokine-cytokine receptor interaction, TGF-/TLR/Jak-STAT signalling and ECM-receptor interaction were targeted. This in vitro study provides a comprehensive molecular insight into the antirheumatic drug response signatures in human chondrocytes, thereby revealing potential molecular targets, pathways and mechanisms of drug action involved in chondrocyte regeneration. Thus, the present study may contribute to the development of novel therapeutic chondro-protective compounds and strategies.
Publication Title
Antirheumatic drug response signatures in human chondrocytes: potential molecular targets to stimulate cartilage regeneration.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
To study the gene expression profile of salivary glands with varying degrees of inflammation in Sjogren's and non Sjogren's patients
Publication Title
Chitinases in the salivary glands and circulation of patients with Sjögren's syndrome: macrophage harbingers of disease severity.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
We have studied the expression profile of 3D cultured human chondrocytes that were stimulated with supernatant of synovial fibroblasts derived from a RA patient (RASF=HSE cell line) and from a normal donor (NDSF=K4IM cell line), respectively. For this purpose, passage 2 human chondrocytes were cultured for 14 days in alginate beads and subsequently stimulated for 48 hours with supernatant of RASF and NDSF. Baseline expression was determined of unstimulated chondrocytes. Differential genome-wide microarray analysis of RASF and NDSF stimulated chondrocytes disclosed a distinct expression profile related to cartilage destruction involving marker genes of inflammation (COX-2), NF-kappa B signaling pathway (TLR2), cytokines/chemokines and receptors (CXCL1-3, CCL20, CXCL8, CXCR4, IL-6, IL-1beta), matrix degradation (MMP-10, MMP-12) and suppressed matrix synthesis (COMP). Thus, transcriptome profiling of RASF and NDSF stimulated chondrocytes revealed a disturbed catabolic-anabolic homeostasis of chondrocyte function. This study provides a comprehensive insight into the molecular regulatory processes induced in human chondrocytes during RA-related cartilage destruction.
Publication Title
Key regulatory molecules of cartilage destruction in rheumatoid arthritis: an in vitro study.
Sample Metadata Fields
No sample metadata fields
View Samples