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SRP067173
Homo sapiens
10 Downloadable Samples
IlluminaHiSeq2500
Description
LMO2 is a component of multisubunit DNA-binding transcription factor complexes that regulate gene expression in hematopoietic stem and progenitor cell development. Enforced expression of LMO2 causes leukemia by inducing hematopoietic stem cell-like features in T-cell progenitor cells, but the biochemical mechanisms of LMO2 function have not been fully elucidated. In this study we systematically dissected the LMO2/LDB1 binding interface to investigate the role of this interaction in T-cell leukemia. Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif R320LITR required for LMO2 binding. Most strikingly, co-expression of full length, wild type LDB1 increased LMO2 steady state abundance, whereas co-expression of mutant proteins deficient in LMO2 binding compromised LMO2 stability. These mutant LDB1 proteins also exerted dominant negative effects on growth and transcription in diverse leukemic cell lines. Raw gene expression data on HSB-2 cells is presented here. Overall design: RNAseq were performed on HSB cell lines to examine their expression patterns
Publication Title
LMO2 Oncoprotein Stability in T-Cell Leukemia Requires Direct LDB1 Binding.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
TRF2 is a paralogue of TATA-box binding protein (TBP) with highest expression in testis. Although Trf2 inactivation in mice leads to arrested spermatogenesis, there is no direct evidence that Trf2 is recruited to chromatin to directly regulate gene expression. We used genetically modified mice where endogenous Trf2 has been modified to carry a TAP-TAG to perform ChIP-reChIP followed by deep sequencing. We found that Trf2 is recruited to all active promoters as a subunit of TFIIA/ALF complex together with TBP. To assess the effect of Trf2 inactivation on gene expression we performed RNA-seq on WT and Trf2-/- testes at 21 days of age when haploid cell gene expression is activated. Overall design: The testes from three 21 day old WT and three Trf2-/- males were taken to prepare total RNAs for deep sequencing.
Publication Title
TRF2 is recruited to the pre-initiation complex as a testis-specific subunit of TFIIA/ALF to promote haploid cell gene expression.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
In this study we demonstrate that Tgif1 has a role in HSCs maintenance, self-renewal and quiescence. RNA sequencing data of LSK cells (HSCs enriched cell population) from Tgif1-/- and wild type mice implicates that multiple pathways involved in HSC quiescence and self-renewal are disturbed in Tgif1 deficient mice. Overall design: RNA expression profiles of wild type (WT) and Tgif1-/- LSK cells were generated by RNA sequencing, in triplicate, using Illumina HiSeq 2000.
Publication Title
Tgif1 regulates quiescence and self-renewal of hematopoietic stem cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 14 Downloadable Samples
- Illumina HiSeq 2000
Description
Identify genes which are induced in wild type, crel ko, and relbcrle dbko B cells under BAFF stimulation, and find the differential expressed genes which are distinct from wildtype controls. Overall design: RNA-seq analysis of wild type, crelko, relbcrel dbko follicular B cells stimulated with BAFF ligand for 6 hours and wildtype only for 27 hours
Publication Title
B-cell survival and development controlled by the coordination of NF-κB family members RelB and cRel.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 11 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
H929 human myeloma cells were exposed to aminopeptidase inhibitor (CHR-2797), HDAC inhibitor (CHR-3996), or a combinaion of the two agents, for 24 hours.
Publication Title
The combination of HDAC and aminopeptidase inhibitors is highly synergistic in myeloma and leads to disruption of the NFκB signalling pathway.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 13 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Thymic lymphomas develop spontaneously in LN3 mice. As for T-ALL in general, ex vivo LN3 lymphoma cells require stromal support to remain viable in culture. We found that primary stromal cells from thymic lymphomas, but not from wild-type thymi, support ex vivo lymphoma survival. By FACS sorting stromal populations, we identified dendritic cells in the tumor microenvironment as the cells capable of supporting lymphoma survival.
Publication Title
Endogenous dendritic cells from the tumor microenvironment support T-ALL growth via IGF1R activation.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2500
Description
Our goal was to identify early genetic changes in the development of autoimmune dysfunction. WT and IL-2-KO CD8 T cells were sorted from the lymph node and spleen of 12-day old mice. Total RNA was isolated by Expression Analysis Inc. using Illumina TrueSeq Stranded Total RNA Sample Preparation Kit. Eight samples were sequenced (four biological replicates of IL-2-KO and WT/HET mice), producing 2X50 paired-end reads using the Illumine HiSeq 2500 platform. Raw reads were provided by Expression Analysis. We identified several genetic signatures within the bulk data including a cytolyic pattern and a novel gene expression pattern indicating a helper-like function. Overall design: WT and IL-2-KO CD8 T cells were sorted from the lymph node and spleen of 12-day old mice. Total RNA was isolated by Expression Analysis Inc. using Illumina TrueSeq Stranded Total RNA Sample Preparation Kit. Eight samples were sequenced (four biological replicates of IL-2-KO and WT/HET mice).
Publication Title
CD8 Follicular T Cells Promote B Cell Antibody Class Switch in Autoimmune Disease.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 35 Downloadable Samples
- Illumina HiSeq 2000
Description
Bipolar disorder (BD) is a highly heritable and heterogeneous mental illness whose manifestations often include impulsive and risk-taking behavior. This particular phenotype suggests that abnormal striatal function could be involved in BD etiology, yet most transcriptomic studies of this disorder have concentrated on cortical brain regions. We report the first transcriptome profiling by RNA-Seq of the human dorsal striatum comparing bipolar and control subjects. Differential expression analysis and functional pathway enrichment analysis were performed to identify changes in gene expression that correlate with BD status. Further co-expression and enrichment analyses were performed to identify sets of correlated genes that show association to BD. Overall design: Total RNA samples were isolated from 36 postmortem dorsal striatum subjects (18 bipolar and 18 control) and sequenced. One outlier sample was removed and 35 samples (18 bipolar and 17 control) were analyzed.
Publication Title
Transcriptome sequencing implicates dorsal striatum-specific gene network, immune response and energy metabolism pathways in bipolar disorder.
Sample Metadata Fields
Sex, Subject
View Samples- Mus musculus
- 17 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Duchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse model of DMD can prevent dystrophic pathophysiology. Physiological tests showed that the transgenic mouse muscle functioned in a way similar to normal muscle. More recently, it has become possible to analyse disease pathways using microarrays, a sensitive method to evaluate the efficacy of a therapeutic approach. We thus examined the gene expression profile of mdx mouse muscle compared to normal mouse muscle and compared the data with that obtained from the transgenic line expressing utrophin. The data confirm that the expression of utrophin in the mdx mouse muscle results in a gene expression profile virtually identical to that seen for the normal mouse. This study confirms that a strategy to up-regulate utrophin is likely to be effective in preventing the disease.
Publication Title
Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for dystrophin deficiency.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Developmental morphogenesis, tissue injury, and oncogenic transformation can cause the detachment of epithelial cells. These cells are eliminated by a specialized form of apoptosis (anoikis). While the processes that contribute to this form of cell death have been studied, the underlying mechanisms remain unclear. Here we tested the role of the cJUN NH2-terminal kinase (JNK) signaling pathway using murine models with compound JNK-deficiency in mammary and kidney epithelial cells. These studies demonstrated that JNK is required for efficient anoikis in vitro and in vivo. Moreover, JNK-promoted anoikis required pro-apoptotic members of the BCL2 family of proteins. We show that JNK acts through a BAK/BAX-dependent apoptotic pathway by increasing BIM expression and phosphorylating BMF leading to death of detached epithelial cells. Overall design: In order to understand the role of the JNK pathway in anoikis, Rosa-CreER (Control) and Jnk1flox/flox Jnk2-/- Rosa-CreER (Jnk1-/-Jnk2-/-) cells were grown as attached monoloayers or suspended for 4 hours. RNA was isolated from these cells and subjected to RNASeq to measure differential gene expression. Three separate samples from each condition were analyzed.
Publication Title
JNK Promotes Epithelial Cell Anoikis by Transcriptional and Post-translational Regulation of BH3-Only Proteins.
Sample Metadata Fields
Cell line, Subject
View Samples