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GSE12536
Mus musculus
6 Downloadable Samples
Description
Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs and commited progenitors.
Publication Title
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 5 Downloadable Samples
Description
Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs.
Publication Title
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 1 Downloadable Sample
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Hematopoietic stem cell function and survival depend on c-Myc and N-Myc activity.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
Description
Sialic acids on vertebrate cell surfaces mediate many biological roles. Altered expression of certain sialic acid types or their linkages can have prognostic significance in human cancer. A classic but unexplained example is enhanced 2-6-sialylation on N-glycans, resulting from over-expression of the Golgi enzyme -galactoside:2-6-sialyltransferase (ST6Gal-I). Previous data supporting a role for the resulting Sia2-3Gal1-4GlcNAc (Sia6LacNAc) structure in tumor biology were based on in vitro studies in transfected carcinoma cells, in which increased Sia6LacNAc on 1-integrins enhanced their binding to ligands, and stimulated cell motility. Here we examine for the first time the in vivo role of the ST6Gal-I enzyme in the growth and differentiation of spontaneous mammary cancers in mice transgenic for an MMTV-promoter-driven polyoma-middle-T antigen, a tumor in which beta1-integrin function is important for tumorigenesis, and in maintaining the proliferative state of tumor cells. Tumors induced in St6gal1 null animals were more differentiated in comparison to those in the wild-type background, both by histological analysis and by protein expression profiles. Furthermore, we show the St6gal1 null tumors have selectively altered expression of genes associated with focal adhesion signaling, and have decreased phosphorylation of FAK, a downstream target of 1-integrins. This first in vivo evidence for a role of ST6Gal-I in tumor progression was confirmed using a novel approach, which conditionally restored St6gal1 in cell lines derived from the null tumors. These findings indicate a role for ST6Gal-I as a mediator of tumor progression, with its expression causing a less differentiated phenotype, via enhanced 1-integrin function.
Publication Title
alpha 2-6-Linked sialic acids on N-glycans modulate carcinoma differentiation in vivo.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 7 Downloadable Samples
Description
Over expression of MHC Class l protein in skeletal muscle causes myositis. Phenotype after expression in young mice is more severe.
Publication Title
Overexpression of MHC class I heavy chain protein in young skeletal muscle leads to severe myositis: implications for juvenile myositis.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 1 Downloadable Sample
Description
Diabetogenic CD8+ G9C8 clone cells and the T cells from a transgenic mouse bearing the same TCR as the clone, displayed differences in their ability to induce disease in vivo.Microarray analysis was done to identify the molecular basis for such differences between the two sets of CD8 T cells.
Publication Title
Cytotoxic mechanisms employed by mouse T cells to destroy pancreatic β-cells.
Sample Metadata Fields
Specimen part, Disease
View Samples- Mus musculus
- 218 Downloadable Samples
Description
Ischemic tolerance can be induced by numerous preconditioning stimuli, including various Toll-like receptor (TLR) ligands. We have shown previously that systemic administration of the TLR4 ligand, lipopolysaccharide (LPS) or the TLR9 ligand, unmethylated CpG ODNs prior to transient brain ischemia in mice confers substantial protection against ischemic damage. To elucidate the molecular mechanisms of preconditioning, we compared brain and blood genomic profiles in response to preconditioning with these TLR ligands and to preconditioning via exposure to brief ischemia.
Publication Title
Multiple preconditioning paradigms converge on interferon regulatory factor-dependent signaling to promote tolerance to ischemic brain injury.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Saccharomyces cerevisiae
- 25 Downloadable Samples
Illumina HiSeq 2500
Description
Depletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Publication Title
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Sample Metadata Fields
Genetic information, Subject
View Samples- Saccharomyces cerevisiae
- 25 Downloadable Samples
- Illumina HiSeq 2500
Description
Depletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Publication Title
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Sample Metadata Fields
Genetic information, Subject
View Samples- Saccharomyces cerevisiae
- 25 Downloadable Samples
- Illumina HiSeq 2500
Description
Depletion of essential nutrients triggers regulatory programs that prolong cell growth and survival. Starvation-induced processes increase nutrient transport, mobilize nutrient storage, and recycle nutrients between cellular components. This leads to an effective increase in intracellular nutrients, which may act as a negative feedback that down-regulates the starvation program. To examine how cells overcome this potential instability, we followed the transcription response of budding yeast transferred to medium lacking phosphate. Genes were induced in two temporal waves. The first wave was stably maintained and persisted even upon phosphate replenishment, indicating a positive feedback loop. This commitment was abolished after two hours with the induction of the second expression wave, coinciding with the reduction in cell growth rate. We identify genes that mediate this loss of commitment, and show that the overall temporal stability of the expression response depends on the sequential pattern of gene induction. Our results emphasize the key role of gene expression dynamics in optimizing cellular adaptation. Wild type cells were grown at high Phosphate medium, washed and transferred to no phosphate medium. Sample were taken every 15 minuets for 6 hours Overall design: 25 samples were taken during the time course. Expression data was normalized to the first time point (cells grown at high phosphate medium)
Publication Title
Sequential feedback induction stabilizes the phosphate starvation response in budding yeast.
Sample Metadata Fields
Genetic information, Subject
View Samples