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GSE17880
Mus musculus
43 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The role of hypoxia in 2-butoxyethanol-induced hemangiosarcoma.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Mus musculus
- 56 Downloadable Samples
Description
Mice were treated with either 100mg/kg baclofen or 0.5% methylcellulose alone by oral gavage for 1 or 5 days.
Publication Title
The role of hypoxia in 2-butoxyethanol-induced hemangiosarcoma.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Mus musculus
- 43 Downloadable Samples
Description
Mice were dosed with 2-BE (900mg/kg) or vehicle by oral gavage and sacrificied either after 4 hours of a single dose or after 7 days of daily dosing.
Publication Title
The role of hypoxia in 2-butoxyethanol-induced hemangiosarcoma.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Mus musculus
- 2 Downloadable Samples
Description
The Ag receptors on alpha/beta and gamma/delta T cells differ not only in the nature of the ligands that they recognize but also in their signaling potential. We hypothesized that the differences in alpha/beta - and gamma/delta TCR signal transduction were due to differences in the intracellular signaling pathways coupled to these two TCRs. To investigate this, we employed transcriptional profiling to identify genes encoding signaling molecules that are differentially expressed in mature alpha/beta and gamma/delta T cell populations. Unexpectedly, we found that B lymphoid kinase (Blk), a Src family kinase expressed primarily in B cells, is expressed in gamma/delta T cells but not in alpha/beta T cells. Analysis of Blk-deficient mice revealed that Blk is required for the development of IL-17-producing gamma/delta T cells. Furthermore, Blk is expressed in lymphoid precursors and, in this capacity, plays a role in regulating thymus cellularity during ontogeny.
Publication Title
Unexpected role for the B cell-specific Src family kinase B lymphoid kinase in the development of IL-17-producing γδ T cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 40 Downloadable Samples
Description
This represents an unbiased evaluation of the transcriptional response in the prefrontal cortex and hippocampus areas in the Df(16)A/+ mice, a mouse model of human 22q11 microdeletion syndrome. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1
Publication Title
Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Description
We present a robust serum-free system for the rapid and efficient reprogramming of mouse somatic cells by Oct4, Sox2 and Klf4. The elimination of fetal bovine serum and oncogene c-Myc allowed reprogramming cells to be detected as early as Day 2 and reached greater than 10% of the population at Day 7 post retroviral transduction. The resulting iPS colonies were isolated with high efficiency to establish pluripotent cell lines. Based on this method, we further developed iPS-SF1 as a dedicated reprogramming medium for chemical screening and mechanistic investigations.
Publication Title
Towards an optimized culture medium for the generation of mouse induced pluripotent stem cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Extensive molecular profiling of leukemias and preleukemic diseases has revealed that distinct clinical entities, like acute myeloid (AML) and T-lymphoblastic leukemia, share the same pathogenetic mutations. It is not well understood how the cell of origin, accompanying mutations, extracellular signals or structural differences in a mutated gene determine the phenotypic identity of the malignant disease. We studied the relationship of different protein domains of the MN1 oncogene and their effect on the leukemic phenotype, building on the ability of MN1 to induce leukemia without accompanying mutations. We found that the most C-terminal domain of MN1 was required to block myeloid differentiation at an early stage, and deletion of an extended C-terminal domain resulted in loss of myeloid identity and cell differentiation along the T-cell lineage in vivo. Megakaryocytic/erythroid lineage differentiation was blocked by the most N-terminal domain. In addition, the N-terminus was required for proliferation and leukemogenesis in vitro and in vivo through upregulation of HoxA9, HoxA10 and Meis2. Our results provide evidence that a single oncogene can modulate cellular identity of leukemic cells based on its active domains. It is therefore likely that different mutations in the same oncogene may impact cell fate decisions and phenotypic appearance of malignant diseases.
Publication Title
Cell fate decisions in malignant hematopoiesis: leukemia phenotype is determined by distinct functional domains of the MN1 oncogene.
Sample Metadata Fields
Specimen part
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