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GSE29453
Mus musculus
8 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Total bone marrow (BM) from miR-223 knockout (mir-223-/-) and wildtype (miR-223+/+) mice 21 was extracted, prestimulated for 2 days. Then, the BM cells were simultaneously cotransduced with MSCV-Hoxa9-pgk-neomycin and a MSCV-Meis1-IRES-YFP by co-cultivation with irradiated (4,000 cGy) viral producers. HoxA9-Meis1 transduced cells were sorted for YFP expression and continuously selected with neomycin (1.4 mg/ml).
Publication Title
Comprehensive analysis of mammalian miRNA* species and their role in myeloid cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 19 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The accumulation of intramyocellular lipid (IMCL) is recognized as an important determinant of insulin resistance, and is increased by a high-fat diet (HFD). However, the effects of HFD on IMCL and insulin sensitivity are highly variable.
Publication Title
Increased intramyocellular lipid/impaired insulin sensitivity is associated with altered lipid metabolic genes in muscle of high responders to a high-fat diet.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Breast cancer is a curable disease if it is diagnosed at an early stage. However, only little options are left once the tumor is metastasized to distant organs, and more than 90% of breast cancer death is attributed to metastatic disease. The process of metastasis is highly complex and involves many steps for successful colonization of tumor cells at a target organ. According to the cancer stem cell (CSC) theory, which still remains a hypothesis, these metastatic cells must have stem cell-like capability for their self-renewal in addition to their invasive ability. Therefore, it has been predicted that a metastatic stem cell, which is distinct from a cancer stem cell, must exist in the primary tumor mass. To identify genes that are involved in metastasis of CSCs, we isolated CSC populations from a well-established model cell line of breast cancer, MDA-MB231, and that of highly metastatic variants, 231BoM-1833 and 231BrM-2a, using CD24, CD44 and EpCAM (ESA), which have been identified as surface markers for CSCs in breast cancers. Overall yield of CSCs from these cells ranged from 2% to 4%. We then performed global expression profile analysis for these CSCs using the Affymetrix Human Gene 1.0ST array.
Publication Title
Hyaluronan synthase HAS2 promotes tumor progression in bone by stimulating the interaction of breast cancer stem-like cells with macrophages and stromal cells.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 22 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Comparative analysis of cerebellar gene expression changes occurring in Sca1154Q/2Q and Sca7266Q/5Q knock-in mice
Publication Title
The insulin-like growth factor pathway is altered in spinocerebellar ataxia type 1 and type 7.
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 11 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Spinocerebellar ataxia type 6 (SCA6) is a dominantly inherited neurodegenerative disease caused by an expansion of a CAG repeat encoding a polyglutamine (PolyQ) tract in the Cav2.1 voltage-gated calcium channel. Pathologically, it is characterized by selective degeneration of cerebellar Purkinje cells (PCs), which are a common target for PolyQ-induced toxicity among several different SCAs. Mutant Cav2.1 confers toxicity mainly through a toxic gain-of-function mechanism, but subcellular site of expanded Cav2.1 toxicity is controversial and it remains elusive whether SCA6 shares pathogenic cascades with other SCAs. To gain insight into these problems, we studied the cerebellar gene expression patterns of young Sca6 MPI 118Q/118Q knockin (KI) mice, which express mutant Cav2.1 from endogenous locus and faithfully models human SCA6. Comparison of transcriptional changes with those of Sca1 154Q/2Q mice, a faithful KI mouse model of SCA1, revealed that transcriptional signatures in the MPI 118Q/118Q were distinct from those of Sca1 154Q/2Q. Examination of temporal profiles of candidate genes showed that upregulation of those associated with microglial activation was initiated before PC degeneration was apparent and augmented as the disease progressed. Histological analysis of the MPI 118Q/118Q cerebellum confirmed the presence of Iba-1 positive activated microglia. Moreover, predominance of M1-like pro-inflammatory microglia was observed and was concomitant with the increased expression of pro-inflammatory cytokines. These results suggest that the unique transcriptional response, which highlights upregulation of neuroinflammatory genes possibly associated with lysosomal involvement, may play a pivotal role in the pathogenesis. Modulation of innate immune system could pave the way for slowing the progression of SCA6.
Publication Title
Loss of MyD88 alters neuroinflammatory response and attenuates early Purkinje cell loss in a spinocerebellar ataxia type 6 mouse model.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To clarify the functional role of migratory liver-resident leukocytes (LRLs) in the pre-metastatic lung, we identify differentially expressed genes and address biological significance in the liver.
Publication Title
Hepato-entrained B220<sup>+</sup>CD11c<sup>+</sup>NK1.1<sup>+</sup> cells regulate pre-metastatic niche formation in the lung.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To understand the molecular mechanisms mediating Liver Resident Leukocytes (LRL) relocalization from the liver to the lungs in response to tumor progression, isolated LRLs from the liver and lungs of tumor-stimulating mice using a cell sorter. LRLs remaining in the liver displayed increased liver signature when compared to those that migrated into the lungs.
Publication Title
Hepato-entrained B220<sup>+</sup>CD11c<sup>+</sup>NK1.1<sup>+</sup> cells regulate pre-metastatic niche formation in the lung.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We screened a number of interferon inducible genes that may be involved in impeding HBV replication and found an anti-HBV activity in ISG20. ISG20 is an IFN-inducible 3- to 5-exonuclease, that degrades DNA and RNA and reduces antigen production in hepatocyte-derived cells
Publication Title
Interferon-stimulated gene of 20 kDa protein (ISG20) degrades RNA of hepatitis B virus to impede the replication of HBV in vitro and in vivo.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We identified SLC44A5 as a gene associated with birth weight in cattle based on genome wide association studies.
Publication Title
The molecular effects of a polymorphism in the 5'UTR of solute carrier family 44, member 5 that is associated with birth weight in Holsteins.
Sample Metadata Fields
Cell line
View Samples- Schizosaccharomyces pombe
- 2 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
In examining NO signaling in the fission yeast Schizosaccharomyces pombe, we found that the putative NO dioxygenase SPAC869.02c (named Yhb1) and the S-nitrosoglutathione reductase Fmd2 cooperatively reduced intracellular NO levels as NO-detoxification enzymes. Although both protein levels were increased with exogenous NO, their expression patterns were different during growth phases. While expression of Yhb1 in the log phase was abrogated by treatment with an NO synthase inhibitor, induction of Fmd2 in the stationary phase was correlated with elevated mitochondrial respiratory chain (MRC) activity and reactive oxygen species (ROS) generation. Moreover, NO was localized in the mitochondria specifically in the stationary phase, suggesting that there are at least two distinctive types of NO signaling in S. pombe cells. For mitochondrial NO signaling, pretreatment with an NO donor effectively rescued the cell viability by repressing generation of ROS under oxidative stress. DNA microarray analysis revealed that exogenous NO contributes to tolerance to hydrogen peroxide (H2O2) stress by (i) inhibition of Fe3+ to Fe2+conversion, (ii) upregulation of the H2O2-detoxifying enzymes, and (iii) downregulation of the MRC genes. Therefore, NO is suggested to play a pivotal role in the negative feedback system to regulate ROS levels under oxidative stress in S. pombe cells.
Publication Title
Nitric oxide signaling and its role in oxidative stress response in Schizosaccharomyces pombe.
Sample Metadata Fields
Treatment
View Samples