Filters
Technology
Platform
Mus musculus
26 Downloadable Samples
NextSeq 500
Description
Experience-dependent plasticity (EDP) is essential for anatomical and functional maturation of sensory circuits during development and can be readily studied is the rodent barrel cortex. Using this model we aimed to uncover changes on the transcriptome level and applied RNA sequencing upon altered sensory experience in juvenile mice in a cortical column and layer specific manner. From column- and layer-specific barrel cortical tissue, high quality RNA was purified and sequenced. The current dataset entails an average of 50 million paired-end reads per sample, 75 base pairs in length. Overall design: Wild type mice were deprived of their C-row whiskers from P12 until P23-P24, after which acute brain slices were prepared and tissues were excised from L2/3 and L4 from specific barrel columns. RNA isolated from these tissue sections was then subjected to RNA-sequencing.
Publication Title
Transcriptional mapping of the primary somatosensory cortex upon sensory deprivation.
Sample Metadata Fields
Cell line, Subject
View Samples
SRP159079- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
Human Tregs isolated from PBMCs were cultured in the absence or presence of IL-12 (20ng/ml) for four days and were performed mRNA-seq. Overall design: mRNA profiles of human Treg stimulated with IL-12 (Th1 condition)
Publication Title
Activated β-catenin in Foxp3<sup>+</sup> regulatory T cells links inflammatory environments to autoimmunity.
Sample Metadata Fields
Age, Subject
View Samples GSE8481- Homo sapiens
- 63 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
We performed the GeneChip analysis to identify multiple extracellular determinants such as cytokines, cell membrane-bound molecules, and matrix responsible for cardiomyogenic differentiation, and evaluated the statistical significance of differential gene expression by the NIA array analysis (http://lgsun.grc.nia.nih.gov/ANOVA/) (Bioinformatics 21: 2548), a web-based tool for microarrays data analysis.
Publication Title
Gremlin enhances the determined path to cardiomyogenesis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2500
Description
We report the first RNA-Seq experiments profiling the effects of DEK loss in HNSCC. Our data also incorporates HPV+ and HPV- tumors to idenfity HPV-dependent and -independent gene signatures. Overall design: RNA-Seq of DEK-dependent gene signatures in HNSCC cell lines
Publication Title
IRAK1 is a novel DEK transcriptional target and is essential for head and neck cancer cell survival.
Sample Metadata Fields
No sample metadata fields
View Samples GSE75058- Mus musculus, Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 11 Downloadable Samples
- Illumina HiSeq 2500
Description
We performed whole genome expression analysis using BCR/ABL expressing Kit+ cells derived from wild type and ROSACreERT2c-Fosfl/flDusp1-/- bone marrow cells. Wild type kit+ cells were treated with DFC+BCI and DFC+BC+Im to mimic the genetic loss of c-Fos and Dusp1. Overall design: The experiment was designed to test whether chemical inhibition by FOS and Dusp1 Inhibitor mimics the genetic deletion of cFOS and Dusp1 in mouse primary cells transduced with BCR-ABL. This data is part of the super series Mechanism of Oncogene addiction GSE75058.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The Baf3 are dependent on IL-3 for grwoth however transformation by BCR -ABL oncogene causes BAf3 cells independent of IL-3. The BAf3 cells expressing BCR-ABL are dependent on continuous expression of BCR_ABL for growth. Inhibitionof BCR-ABL by its inhibitor Imatinib cause these cells to undergo apoptosis. When these cells are grown with IL-3 these cells do not respond to Imatinib mediated grwoth arrest.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
K562 cells when grown with erythropeitin do not respond to Imatinib. Here we are comparing the gene expression profile from imatinib resistant and sensitive cells.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
BAF3 cells harboring constitutively expressing BCR-ABL were grown with or without IL-3 supplement and treated with Imatinib and live cells from the IL-3 and without IL-3 were sorted by FACS.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 27 Downloadable Samples
- Illumina HiSeq 1000
Description
Inhibition of mTOR signaling using the rapalog everolimus is an FDA-approved targeted therapy for patients with lung and gastroenteropancreatic neuroendocrine tumors (NET). However, patients eventually progress on treatment, highlighting the need for additional therapies. We focused on pancreatic NETs (pNETs) and reasoned that treatment of these tumors upon progression on rapalog therapy, with an mTOR kinase inhibitor (mTORKi) such as CC-223 could overcome a number of resistance mechanisms in tumors and delay cardiac carcinoid disease. We performed preclinical studies using human pNET cells in vitro and injected them subcutaneously or orthotopically to determine tumor progression and cardiac function in mice treated with either rapamycin alone or switched to CC-223 upon progression. Detailed signaling and RNA sequencing analyses were performed on tumors that were sensitive or progressed on mTOR treatment. Approximately 57% of mice bearing pNET tumors which progressed on rapalog therapy showed a significant decrease in tumor volume upon a switch to CC-223. Moreover, mice treated with an mTORKi exhibited decreased cardiac dilation and thickening of heart valves than those treated with placebo or rapamycin alone. In conclusion, in the majority of pNETs that progress on rapalogs, it is possible to reduce disease progression using an mTORKi, such as CC-223. Moreover, CC-223 had an additional transient cardiac benefit on valvular fibrosis compared to placebo- or rapalog-treated mice. These results provide the preclinical rationale to further develop mTORKi clinically upon progression on rapalog therapy and to further test their long term cardioprotective benefit in those NET patients prone to carcinoid syndrome. Overall design: We performed RNA sequencing analyses as an unbiased means to assess changes in gene expression. Our major goal was to identify the differences in tumor mRNAs between the CC-223- and non-CC-223 responders compared to the rapamycin alone treatment arm (Fig 5A in Orr-Asman et al manuscript). The analysis was conducted using 1 tumor each from 13 and 14 mice treated with rapamycin or switched to CC-223 respectively.
Publication Title
mTOR Kinase Inhibition Effectively Decreases Progression of a Subset of Neuroendocrine Tumors that Progress on Rapalog Therapy and Delays Cardiac Impairment.
Sample Metadata Fields
Specimen part, Subject
View Samples