Filters
Technology
Platform
Mus musculus
6 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Common myeloid progenitor cells from murine bone marrow were sorted according to ROS content using FACS with H2-DCFDA staining.
Publication Title
Intracellular reactive oxygen species mark and influence the megakaryocyte-erythrocyte progenitor fate of common myeloid progenitors.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Drug-induced cardiac arrhythmia characterized by QT prolongation and torsade de pointes has been a major reason for drug withdrawal at the late stage of clinical trials. Current preclinical testing is still insufficient to identify drugs with pro-arrhythmic risks. Human induced pluripotent stem cell-derived cardiomyocytes are a promising development in safety screening as a reproducible human model. Using the patch-clamp technique, we showed that human induced pluripotent stem cell-derived cardiomyocytes exhibited spontaneous action potentials, which represent relatively immature forms of cardiac cells. Furthermore, in some spontaneously beating cells, a hERG blocker, E4031, depolarized membrane potentials and stopped spontaneous firing, resulting in failure to evaluate drug effects on electrophysiological parameters that reflect repolarization processes. Here we show that human stem cell-derived cardiomyocytes with transduced KCNJ2 encoding the inward-rectifier potassium channel have characteristics similar to mature cardiomyocytes including responsiveness to rate changes and potassium channel blockers. Our novel strategy could allow implementation of human induced pluripotent stem cell-derived cardiomyocytes in drug safety assessment for cardiac toxicity.
Publication Title
Overexpression of KCNJ2 in induced pluripotent stem cell-derived cardiomyocytes for the assessment of QT-prolonging drugs.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
In order to understand the molecular mechanisms of DN thymocyte development, it may be also of use to clarify how these developmental processes are regulated in terms of their entire gene expression, to which cell differentiation is ultimately ascribed.
Publication Title
Expression profiling of immature thymocytes revealed a novel homeobox gene that regulates double-negative thymocyte development.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Expression of genes related to fibrosis was assessed in the liver of AIM+/+ and AM-/- mice fed a high-fat diet (HFD) for various period. Overall, there was no significant difference in the magnitude of expression of fibrosis-related genes during the steatosis progression.
Publication Title
Circulating AIM prevents hepatocellular carcinoma through complement activation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Evi1 is essential for proliferation of hematopoietic stem cells and implicated in the development of myeloid disorders. Particularly, high Evi1 expression defines one of the largest clusters in acute myeloid leukemia and is significantly associated with extremely poor prognosis. Improvement of the therapeutic outcome of leukemia with activated Evi1 is one of the most challenging issues. However, mechanistic basis of Evi1-mediated leukemogenesis has not been fully elucidated. Here we show that Evi1 directly represses PTEN transcription in the murine bone marrow, which leads to activation of AKT/mTOR signaling. In a murine bone marrow transplantation model, Evi1 leukemia showed remarkable sensitivity to an mTOR inihibitor rapamycin. Furthermore, we found that Evi1 binds to several polycomb group proteins and recruits polycomb repressive complexes for PTEN downregulation, which reveals a novel epigenetic mechanism of AKT/mTOR activation in leukemia. Expression analyses and chromatin immunoprecipitation assays using human samples indicate that our findings in mice models are recapitulated in human leukemic cells. Dependence of Evi1-expressing leukemic cells on AKT/mTOR signaling provides the first example of targeted therapeutic modalities that suppress the leukemogenic activity of Evi1. The PTEN/AKT/mTOR signaling pathway and the Evi1-polycomb interaction can be promising therapeutic targets for leukemia with activated Evi1.
Publication Title
Evi1 represses PTEN expression and activates PI3K/AKT/mTOR via interactions with polycomb proteins.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Huntingtons disease (HD) is a dominantly inherited genetic disease caused by mutant huntingtin (htt) protein with expanded polyglutamine tracts. A neuropathological hallmark of HD is the presence of neuronal inclusions of mutant htt. p62 is an important regulatory protein in selective autophagy, a process by which aggregated proteins are degraded, and it is associated with several neurodegenerative disorders including HD. Here we investigated the effect of p62 depletion in three HD model mice: R6/2, HD190QG and HD120QG mice. We found that loss of p62 in these models led to longer lifespans and reduced nuclear inclusions, although cytoplasmic inclusions increased with polyglutamine length. In mouse embryonic fibroblasts (MEFs) with or without p62, mutant htt with a nuclear localization signal (NLS) showed no difference in nuclear inclusion between the two MEF types. In the case of mutant htt without NLS, however, p62 depletion increased cytoplasmic inclusions. Furthermore, to examine the effect of impaired autophagy in HD model mice, we crossed R6/2 mice with Atg5 conditional knockout mice. These mice also showed decreased nuclear inclusions and increased cytoplasmic inclusions, similar to HD mice lacking p62. These data suggest that the genetic ablation of p62 in HD model mice enhances cytoplasmic inclusion formation by interrupting autophagic clearance of polyQ inclusions. This reduces polyQ nuclear influx and paradoxically ameliorates disease phenotypes by decreasing toxic nuclear inclusions.
Publication Title
Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington's model mice.
Sample Metadata Fields
No sample metadata fields
View Samples
GSE37982- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We generated iPSCs from imatinib-sensitive chronic myelogenous leukemia (CML) patient samples.
Publication Title
Generation of induced pluripotent stem cells from primary chronic myelogenous leukemia patient samples.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
To identify the target genes of Runx1/Cbfb in MLL fusion leukemia, we performed microarray analysis using control and Runx1/Cbfb-deleted MLL-AF9 cells.
Publication Title
Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To identify the target genes of Runx1 in MLL fusion leukemia, we performed microarray analysis using control and Runx1-deficient MLL-ENL leukemia cells.
Publication Title
Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To clarify mineralcorticoid receptor and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.
Publication Title
Induction of 11β-HSD 1 and activation of distinct mineralocorticoid receptor- and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples