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GSE33550
Mus musculus, Homo sapiens
66 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The TLX1 and TLX3 transcription factor oncogenes play an important role in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL)1,2. Here we used reverse engineering of global transcriptional networks to decipher the oncogenic regulatory circuit controlled by TLX1 and TLX3. This Systems Biology analysis defined TLX1 and TLX3 as master regulators of an oncogenic transcriptional circuit governing T-ALL. Notably, network structure analysis of this hierarchical network identified RUNX1 as an important mediator of TLX1 and TLX3 induced T-ALL, and predicted a tumor suppressor role for RUNX1 in T-cell transformation. Consistent with these results, we identified recurrent somatic loss of function mutations in RUNX1 in human T-ALL. Overall, these results place TLX1 and TLX3 atop of an oncogenic transcriptional network controlling leukemia development, demonstrate power of network analysis to identify key elements in the regulatory circuits governing human cancer and identify RUNX1 as a tumor suppressor gene in T-ALL.
Publication Title
Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 59 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Transgenic expression of key transcritpion factors inducing T-cell leukemias in mice.
Publication Title
Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The experiment was designed in order to knock down the expression of TLX3 gene in T-ALL cell line
Publication Title
Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The experiment was designed in order to knock down the expression of TLX1 gene in T-ALL cell line
Publication Title
Disregulated expression of the transcription factor ThPOK during T-cell development leads to high incidence of T-cell lymphomas.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 20 Downloadable Samples
Illumina HiSeq 2000
Description
Reprogramming to pluripotency after overexpression of OCT4, SOX2, KLF4 and MYC is accompanied by global genomic and epigenomic changes. Histone modification and DNA methylation states in iPSCs have been shown to be highly similar with embryonic stem cells (ESCs). However, epigenetic differences still exist between iPSCs and ESCs. In particular, aberrant DNA methylation states found in iPSCs are a major concern for using iPSCs in a clinical setting. Thus, it is critical to find factors that regulate DNA methylation states in reprogramming. Here, we found that the miR-29 family is an important epigenetic regulator during human somatic cell reprogramming. Our global DNA methylation and hydroxymethylation analysis shows that DNA demethylation is a major event mediated by miR-29a depletion during early reprogramming, and that iPSCs derived from miR-29a depletion are epigenetically closer to ESCs. Our findings uncover an important miRNA-based approach to generate clinically robust iPSCs. Overall design: Bisulphite converted gDNAs of D551 fibroblasts transduced for 3 days with overexpression of DNMTs, TETs, TDG and OSKM or miR29a/b/c and control sponge were hybridized into Illumina Infinium HumanMethylation 450K Beadchip.
Publication Title
Regulation of the DNA Methylation Landscape in Human Somatic Cell Reprogramming by the miR-29 Family.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Rattus norvegicus
- 28 Downloadable Samples
- Illumina HiSeq 2500
Description
The pancreatic beta cell function failure is the core event of type 2 diabetes mellitus. High levels of free fatty acid and glucose are two main factor that induced pancreatic beta cell function failure. Long term exposure to palmitate can induced pancreatic beta cell apoptoss and impaired insulin secretion in vivo and in vitro, called lipotoxicity. The lipotoxicity often coupled with high glucose, their combination form called glucolipotoxcity. We carried out temporal transcriptome and proteome studies investigating the evolution of molecular events in Ins1 cells stimulated by palmitate for different times. And through compared the transcriptome and proteome between lipotoxicity and glucolipotoxicity explain the mechanism of glucolipotoxicity more harmfull to beta cell. Overall design: we performed a time-course large-scale transcriptome of INS1 cells induced by 0.5 mM palmitate and 0.5 mM palmitate with 27.8 mM glucose at four time points (8, 16, 24 and 48 h) using MAPS method
Publication Title
Temporal Proteomic Analysis of Pancreatic β-Cells in Response to Lipotoxicity and Glucolipotoxicity.
Sample Metadata Fields
Specimen part, Cell line, Subject, Time
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Compare with normal nasopharyngeal epithelial cells, we found ACAT1 was decreased in NPC cells, we found that ACAT1 inhibited proliferation, colony formation, migration and invasion in NPC cells. We used microarrays to identify differential genes regulated by ACAT1 in NPC cell lines.
Publication Title
Epigenetic Inactivation of Acetyl-CoA Acetyltransferase 1 Promotes the Proliferation and Metastasis in Nasopharyngeal Carcinoma by Blocking Ketogenesis.
Sample Metadata Fields
Cell line, Treatment
View Samples- Oryza sativa
- 6 Downloadable Samples
- Affymetrix Rice Genome Array (rice)
Description
In order to study the function of CHR729 in rice, the T-DNA insertion mutant of CHR729 was obtained and analysed.
Publication Title
CHD3 protein recognizes and regulates methylated histone H3 lysines 4 and 27 over a subset of targets in the rice genome.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
The oscillation status of the circadian clock during late gestation is not clear. To gain a better understanding on the oscillation state of the clock and possible influences by maternal cues, we performed transcriptome analyses on the fetal liver tissue during late gestation.
Publication Title
Circadian rhythms of fetal liver transcription persist in the absence of canonical circadian clock gene expression rhythms in vivo.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 6 Downloadable Samples
- IlluminaHiSeq2000
Description
Novel analytic tools are needed to elucidate the molecular basis of leukemia-relevant gene mutations in the post-genome era. We generated isogenic leukemia cell clones in which the FLT3 gene was disrupted in a single allele using TALENs. Isogenic clones with mono-allelic disrupted FLT3 were compared to an isogenic wild-type control clone and parental leukemia cells for transcriptional expression, downstream FLT3 signaling and proliferation capacity. The global gene expression profiles of mutant K562 clones and corresponding wild-type controls were compared using RNA-seq. The transcriptional levels and the ligand-dependent autophosphorylation of FLT3 were decreased in the mutant clones. TALENs-mediated FLT3 haplo-insufficiency impaired cell proliferation and colony formation in vitro. These inhibitory effects were maintained in vivo, improving the survival of NOD/SCID mice transplanted with mutant K562 clones. Cluster analysis revealed that the gene expression pattern of isogenic clones was determined by the FLT3 mutant status rather than the deviation among individual isogenic clones. Differentially expressed genes between the mutant and wild-type clones revealed an activation of nonsense-mediated decay pathway in mutant K562 clones as well as an inhibited FLT3 signaling. Our data support that this genome-editing approach is a robust and generally applicable platform to explore the molecular bases of gene mutations. Overall design: Global gene expression profiles of three isogenic K562 mutant clones (clones k20, k112, k324) and three randomly selected wild-type clones (clones kw1, kw2, kw3) were generated by RNA-seq, using Illumina Hiseq 2000.
Publication Title
TALENs-mediated gene disruption of FLT3 in leukemia cells: Using genome-editing approach for exploring the molecular basis of gene abnormality.
Sample Metadata Fields
No sample metadata fields
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