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SRP003672
Homo sapiens
12 Downloadable Samples
Illumina Genome Analyzer II
Description
We have used deep sequencing to explore the repertoire of both poly(A)+ and poly(A)- RNAs from two standard cell lines, HeLa cells and human embryonic stem cell (hESC) H9 cells. Overall design: Examination of nonpolyadenylated and polyadenylated in 2 cell types.
Publication Title
Genomewide characterization of non-polyadenylated RNAs.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaGenomeAnalyzerII
Description
We have used deep sequencing to explore the repertoire of both poly(A)+ and poly(A)- RNAs from two standard cell lines, HeLa cells and human embryonic stem cell (hESC) H9 cells. Overall design: Examination of nonpolyadenylated and polyadenylated RNA in 2 cell types.
Publication Title
Genomewide characterization of non-polyadenylated RNAs.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
We describe the discovery of sno-lncRNAs, a class of nuclear-enriched intron-derived long noncoding RNAs (lncRNAs) that are processed on both ends by the snoRNA machinery. During exonucleolytic trimming, the sequences between the snoRNAs are not degraded, leading to the accumulation of lncRNAs flanked by snoRNA sequences but lacking 5'' caps and 3'' poly(A) tails. Such RNAs are widely expressed in cells and tissues and can be produced by either box C/D or box H/ACA snoRNAs. Importantly, the genomic region encoding one abundant class of sno-lncRNAs (15q11-q13) is specifically deleted in Prader-Willi Syndrome (PWS). The PWS region sno-lncRNAs do not colocalize with nucleoli or Cajal bodies, but rather accumulate near their sites of synthesis. These sno-lncRNAs associate strongly with Fox family splicing regulators and alter patterns of splicing. These results thus implicate a previously unannotated class of lncRNAs in the molecular pathogenesis of PWS. Overall design: We have used deep sequencing to explore the gene expression from poly(A)+ RNAs in embryonal carcinoma (EC) line PA-1 cells treated with scrambled or specific antisense oligodeoxynucleotides (ASOs).
Publication Title
Long noncoding RNAs with snoRNA ends.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- Illumina Genome Analyzer II
Description
We used immunoprecipitation to pulldown Lin28 associated RNA targets and used genome-wide high throughput deep sequencing to identified those Lin28-associated RNAs. Keywords: Lin28 IP-RNAseq Overall design: Examination of Lin28 immunoprecipitated RNA transcripts
Publication Title
Genome-wide studies reveal that Lin28 enhances the translation of genes important for growth and survival of human embryonic stem cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- NextSeq 500
Description
Soleus muscle has the most abundant H19 expression compared to other skeletal muscle tissues. In order to identify genes regulated by long noncoding RNA H19 in skeletal muscle, we performed RNA-Seq with dissected WT and H19KO soleus muscles from 21 week old mice. Among the differentially expressed genes, we found skeletal muscle - overexpressed gene DUSP27, which potentially plays an important role in regulating skeletal muscle glucose metabolisim by regulating the activitiy of AMPK, might be a target of H19 mediated regulation. Overall design: Soleus muscle was harvested from 21-week old mice, followed by total RNA extraction, library preparation and RNA-seq analysis to compare trancript profiles between WT and H19KO conditions.
Publication Title
H19 lncRNA Promotes Skeletal Muscle Insulin Sensitivity in Part by Targeting AMPK.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 144 Downloadable Samples
Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)
Description
As part of a larger effort to provide proof-of-concept in vitro only risk assessments, we have developed a suite of high throughput assays for key readouts in the p53 DNA damage response toxicity pathway: DSB DNA damage (p-H2AX), permanent chromosomal damage (micronuclei; MN), p53 activation, p53 transcriptional activity, and cell fate (cell cycle arrest, apoptosis,MN). Dose-response studies were performed with these protein and cell fate assays, together with whole genome transcriptomics, for three prototype chemicals: etoposide (ETP), quercetin (QUE) and methyl methanesulfonate (MMS). Data were collected in a human cell line expressing wild-type p53 (HT1080) and results were confirmed in a second p53 competent cell line (HCT 116). At chemical concentrations causing similar increases in p53 protein expression, p53-mediated protein expression and cellular processes showed substantial chemical-specific differences. These chemical-specific differences in the p53 transcriptional response appear to be determined by augmentation of the p53 response by co-regulators. More importantly, dose-response data for each of the chemicals indicates that the p53 transcriptional response does not prevent MN induction at low concentrations. In fact, the no observed effect levels (NOELs) and benchmark doses (BMDs) for MN induction were less than or equal to those for p53-mediated gene transcription regardless of the test chemical, indicating that p53s post-translational responses may be more important than transcriptional activation in the response to low dose DNA damage. This effort demonstrates the process of defining key assays required for a pathway-based, in vitro-only risk assessment, using the p53-mediated DNA damage response pathway as a prototype.
Publication Title
Profiling dose-dependent activation of p53-mediated signaling pathways by chemicals with distinct mechanisms of DNA damage.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Treatments that stimulate neuronal excitability enhance motor performance after stroke.cAMP-response-element binding protein (CREB) is a transcription factor that plays a key rolein neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool ofmotor neurons enhances motor recovery after stroke, while blocking CREB signaling preventsstroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with thehM4di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue,demonstrating that it is possible to turn off and on stroke recovery by manipulating theactivity of CREB-transfected neurons. CREB transfection enhances re-mapping of injuredsomatosensory and motor circuits, and induces the formation of new connections withinthese circuits. CREB is a central molecular node in the circuit responses after stroke that leadto recovery from motor deficits.
Publication Title
CREB controls cortical circuit plasticity and functional recovery after stroke.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- NextSeq 500
Description
We used high throughput sequencing to compare the differential gene expression of HepG2 cells with and without H19 knockdown. We found critical genes involved in glucose production changed significantly after H19 konckdown compared to control. Overall design: HepG2 cells were transfected with either control siRNA or siH19. 48h after transfection, total RNA was extracted for library preparation and RNA-seq analysis to compare trancript profiles between siCon and siH19 cells.
Publication Title
Elevated hepatic expression of H19 long noncoding RNA contributes to diabetic hyperglycemia.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Pancreatic beta cells use electrical signals to couple changes in blood glucose concentration to insulin release via extracellular calcium (Ca2+) influx. Sorcin (SRI) is a Ca2+-binding protein whose overexpression in cardiomyocytes rescues the abnormal contractile function of the diabetic heart.
Publication Title
Sorcin Links Pancreatic β-Cell Lipotoxicity to ER Ca2+ Stores.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
GATA2 mutants were discovered in families predisposed to MDS/AML and in sporadic cases of CML-blast crisis. Promyelocytic HL-60 cells were transduced with lentiviral vectors that express GATA2 WT or T354M, 355delT or L359V mutants upon addition of 4-hydroxy tamoxifen (4HT). Microarrays were performed to identify GATA2 WT signatures and differences caused by these mutations.
Publication Title
Heritable GATA2 mutations associated with familial myelodysplastic syndrome and acute myeloid leukemia.
Sample Metadata Fields
Specimen part, Cell line
View Samples