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GSE16749
Mus musculus
4 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We used microarrays to understand the effect miR-155 has on osteoclast differentiation.
Publication Title
miRNA-based mechanism for the commitment of multipotent progenitors to a single cellular fate.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 267 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Genetic background may contribute to PAM50 gene expression breast cancer subtype assignments.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 134 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and MOLF/Ei strain. Tumors were harvested from the animals for gene expression analysis to identify genes associated with progression to distant metastatic disease.
Publication Title
Genetic background may contribute to PAM50 gene expression breast cancer subtype assignments.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 133 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and the G5 generation of the Diversity Outcross (DO). Tumors were harvested from the animals for gene expression analysis to identify genes associated with progression to distant metastatic disease.
Publication Title
Genetic background may contribute to PAM50 gene expression breast cancer subtype assignments.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
Illumina HiSeq 2500
Description
The goal of the study was to compare transcriptome changes in HeLa cells after infection with recombinant Thogoto virus (wild-type, ML deletioin mutant or ML SW mutant not able to interact wiith TFIIB. While wild-type virus is able to inhibit inflammatory genes, ML deletion mutant and TFIIB-non-interacting mutant lose this effect on gene transcription. Overall design: Examination of transcriptome changes in HeLa cells under steady state or after THOV infection using Illumina HiSeq.
Publication Title
Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Cells are constantly exposed to stress. Most of those stresses do not necessarily cause cell death or visible damage. The present study explores the way the immune system responds to such sub lethal stressed cells.
Publication Title
Cells exposed to sublethal oxidative stress selectively attract monocytes/macrophages via scavenger receptors and MyD88-mediated signaling.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2000
Description
Phenotypic and functional changes seen in the aged adaptive immune system are primarily driven by aging of hematopoietic stem cells (HSCs), pharmacological rejuvenated aged HSCs were able to reconstituted a youthful immune system Overall design: We employed RNA-seq to assess similarities/differences between naive CD4+ T cells and CD19+ B cells isolated from RAG1-/- recipients transplanted with either young, old or old rejuvenated (CASIN treated) HSCs
Publication Title
Aged murine hematopoietic stem cells drive aging-associated immune remodeling.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
AML1-ETO expression in normal human umbilical cord blood CD34+ cells leads to long-term proliferation of an early self-renewing primitive progenitor cell with multilineage potential and stem cell ability, but these cells do not induce leukemia in immunodeficient mice. This comparative microarray study was initiated to determine the differences in the transcriptome of AML-ETO-expressing CD34+ cells after extended culture in vitro, using normal cord blood cells expanded for 6-8 weeks in vitro and subsequently purified for the CD34+ population as the control comparison.
Publication Title
p53 signaling in response to increased DNA damage sensitizes AML1-ETO cells to stress-induced death.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 16 Downloadable Samples
- IlluminaHiSeq2000
Description
p53 is a pivotal tumor suppressor and a major barrier against cancer. We now report that silencing of the Hippo pathway tumor suppressors LATS1 and LATS2 in non-transformed mammary epithelial cells reduces p53 phosphorylation and increases its association with the p52 NF-?B subunit. Moreover, it partly shifts p53’s conformation and transcriptional output towards a state resembling cancer-associated p53 mutants, and endow p53 with the ability to promote cell migration. Notably, LATS1 and LATS2 are frequently downregulated in breast cancer; we propose that such downregulation might benefit cancer by converting p53 from a tumor suppressor into a tumor facilitator. Overall design: MCF10A cells transfected with siRNA against LATS1/2 alone, p53 alone or LATS1/2 and p53 together. Two independent MCF10A batches provided biological replicates
Publication Title
Down-regulation of LATS kinases alters p53 to promote cell migration.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2500
Description
Senescence is a state of stable cell cycle exit that has important implications for development, physiology and disease. It is distinct from quiescence in which cells can be induced to re-enter the cell cycle. Although it is well known that there are massive changes in the heterochromatin of senescent cells, the molecular mechanisms underpinning the transition from reversible quiescence into irreversible senescence have remained elusive. Here, we demonstrate that the chromatin-remodeling enzyme ATRX is required for senescence. ATRX accumulates in nuclear foci during both replicative and cellular senescence. Using ChIP-seq and RNA-seq we identified HRAS as part of an ATRX regulated gene expression program associated with senescence. Repression of HRAS is sufficient to promote the transition of quiescent cells into senescence. Thus we conclude that the repression of HRAS is likely a direct consequence of ATRX binding and critical to how it mediates its role in senescence. Overall design: mRNA expression profiles were analyzed in dedifferentiated liposarcoma cell lines under cycling, quiescent and senescent (using two unique inducers) conditions via RNA-seq
Publication Title
ATRX is a regulator of therapy induced senescence in human cells.
Sample Metadata Fields
No sample metadata fields
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