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Mus musculus, Homo sapiens
112 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Conserved principles of mammalian transcriptional regulation revealed by RNA half-life.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 45 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Data from tc-, nt- and p-RNA as well as 1 and 2h of actinomycin-D treatment (5g/ml) of NIH-3T3 cells used to determine half-lives. RNA was labeled for 15, 30 or 60 minutes with 4-thiouridine. After preparation of tc-RNA, thiol-labeled RNA was biotinylated using biot-HPDP and subsequently tc-RNA was separated into nt- and p-RNA using streptavidin coated magnetic beads. All three fractions were used for microarray analysis. For actinomycin-D experiments only tc-RNA was used prepared from cell before and 1 an 2h after addition of act-D.
Publication Title
Conserved principles of mammalian transcriptional regulation revealed by RNA half-life.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
RNA was labeled in BL41 cells by culturing cells for 60 min in media containing 100M 4sU. Tc-RNA was separated into nt- and p-RNA. All three RNA subsets were subjected to microarray analysis. Only probe sets providing present calls in all RNA samples/subsets were included into the analysis
Publication Title
Conserved principles of mammalian transcriptional regulation revealed by RNA half-life.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 3 Downloadable Samples
IlluminaHiSeq2000
Description
Huntington’s disease (HD) is a devastating neurological disorder that is caused by an expansion of the poly-Q tract in exon 1 of the Huntingtin gene (HTT). HTT is an evolutionarily conserved and ubiquitously expressed protein that has been linked to a variety of functions including transcriptional regulation, mitochondrial function, and vesicle transport. This large protein has numerous caspase and calpain cleavage sites and can be decorated with several post-translational modifications such as phosphorylations, acetylations, sumoylations, and palmitoylations. However, the exact function of HTT and the role played by its modifications in the cell is still not well understood. Scrutiny of HTT function has been focused on a single, full length, mRNA. In this study, we report the discovery of 5 novel HTT mRNA splice isoforms that are expressed in normal and HD-hESC lines as well as cortical neurons differentiated from hESCs. Interestingly, none of the novel isoforms generates a truncated protein. Instead, 4 of the 5 new isoforms specifically eliminate domains and modifications to generate smaller HTT proteins. The fifth novel isoform incorporates a previously unreported additional exon, dubbed 41b, which is hominid-specific and introduces a potential phosphorylation site in the protein. The discovery of this hominid-specific isoform may shed light on human-specific pathogenic mechanisms of HTT, which could not be investigated with current mouse models of the disease. Furthermore, it provides a new human-specific target for drug screening in Huntington’s disease. Overall design: We performed RNAseq of human embryonic stem cells in pluripotency conditions to check expression of multiple HTT isoforms.
Publication Title
Discovery of novel isoforms of huntingtin reveals a new hominid-specific exon.
Sample Metadata Fields
No sample metadata fields
View Samples
SRP012695- Homo sapiens
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
Analysis of mRNA in THP1 (human monocytic leukemia) cell line in order to correlate miRNA activity with target abundance. Overall design: THP1 mRNA profiles were generated in triplicates by deep-sequencing in Illumina HiSeq2000.
Publication Title
High-throughput assessment of microRNA activity and function using microRNA sensor and decoy libraries.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 35 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Expression data from NIH-3T3 cells treated with mock, 100 U/ml IFN alpha or 100 U/ml gamma for 1 or 3h on nt-RNA labeled for 30-60 min at different times of interferon treatment
Publication Title
High-resolution gene expression profiling for simultaneous kinetic parameter analysis of RNA synthesis and decay.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 23 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2), Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Differential gene expression caused by 1h and 3h of IFN alpha or gamma treatment was analyzed in total cellular RNA of NIH-3T3 cells compared to mock
Publication Title
High-resolution gene expression profiling for simultaneous kinetic parameter analysis of RNA synthesis and decay.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
microRNA-126 is a microRNA predominately expressed by endothelial cells and controls angiogenesis. Unexpectedly, we found that mice deficient in miR-126 have a major impairment in their innate response to pathogen-associated nucleic acids, as well as HIV, which results in more widespread cell infection. Further examination revealed that this was due to miR-126 control of plasmacytoid DC (pDC) homeostasis and function, and that miR-126 regulates expression of TLR7, TLR9, NFkB1 and other innate response genes, as well as VEGF-receptor 2 (VEGFR2). Deletion of VEGFR2 on DCs resulted in reduced interferon production, supporting a role for VEGFR2 in miR-126 regulation of pDCs. These studies identify the miR-126/VEGFR2 axis as an important regulator of the innate response that operates through multiscale control of pDCs.
Publication Title
The miR-126-VEGFR2 axis controls the innate response to pathogen-associated nucleic acids.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Expression data from NIH-3T3 cells left uninfected or infected with MCMV for 2, 4 or 6h on total RNA as well as newly transcribed RNA labeled for 1-2, 3-4, and 5-6hpi. For newly transcribed RNA, the isolated RNA was labeled for 1h and separated from total cellular RNA following Trizol RNA preparation and thiol-specific biotinylation. We used microarrays to analyze the effects of MCMV infection in total and newly transcribed RNA.
Publication Title
Real-time transcriptional profiling of cellular and viral gene expression during lytic cytomegalovirus infection.
Sample Metadata Fields
Disease, Cell line, Time
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
Cytomegaloviruses express large amounts of viral miRNAs during lytic infection, yet, they only modestly alter the cellular miRNA profile. The most prominent alteration upon lytic murine cytomegalovirus (MCMV) infection is the rapid degradation of the cellular miR-27a and miR-27b. Here, we report that this regulation is mediated by the <1.7 kb spliced and highly abundant MCMV m169 transcript. Specificity to miR-27a/b is mediated by a single, apparently optimized, miRNA binding site located in its 3''-UTR. This site is easily and efficiently retargeted to other cellular and viral miRNAs by target site replacement. Expression of the 3''-UTR of m169 by an adenoviral vector was sufficient to mediate its function, indicating that no other viral factors are essential in this process. Degradation of miR-27a/b was found to be accompanied by 3''-tailing and -trimming. Despite its dramatic effect on miRNA stability, we found this interaction to be mutual, indicating potential regulation of m169 by miR-27a/b. Most interestingly, three mutant viruses no longer able to target miR-27a/b, either due to miRNA target site disruption or target site replacement, showed significant attenuation in multiple organs as early as 4 days post infection, indicating that degradation of miR-27a/b is important for efficient MCMV replication in vivo. Overall design: Small RNA sequencing from total RNA or Ago2 associated small RNAs extracted from mock- or MCMV-infected NIH-3T3 cells
Publication Title
Degradation of cellular mir-27 by a novel, highly abundant viral transcript is important for efficient virus replication in vivo.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples