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GSE12075
Mus musculus, Homo sapiens
17 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The impact of microRNAs on protein output.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This array analysis is to study developmental time course of the regulation of target messages expression during culture of murine neutrophils versus miR-223 null neutrophils. Culture media was SILAC-IMDM for MS analysis.
Publication Title
The impact of microRNAs on protein output.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 5 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This array analysis is to study the regulation of target messages expression in murine neutrophils versus miR-223 null neutrophils.
Publication Title
The impact of microRNAs on protein output.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This array analysis is to study the regulation of target messages expression in in vitro cultured murine neutrophils versus miR-223 null neutrophils. Culture media was SILAC-IMDM for MS analysis.
Publication Title
The impact of microRNAs on protein output.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors.
Publication Title
Initiation of myoblast to brown fat switch by a PRDM16-C/EBP-beta transcriptional complex.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Gene expression (mRNA profiling) of U2OS osteosarcoma cells treated with 1 mM of the CDK4/6-specific inhibitor, PD0332991, versus vehicle (DMSO) for 4 hours
Publication Title
A systematic screen for CDK4/6 substrates links FOXM1 phosphorylation to senescence suppression in cancer cells.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 18 Downloadable Samples
Illumina HiSeq 2500
Description
Ubiquilins are a family of proteins involved in proteasomal degradation of mislocalized membrane proteins. Here, Greer et al. demonstrate that Ubqln1 is required for BCR-driven B cell proliferation through maintenance of protein synthesis following stimulation. In the absence of Ubqln1, mitochondrial proteins accumulate in the cytosol, which may account for the observed proteostasis. BCR stimulation of murine B cells induced a long-lasting mitochondrial depolarization that did not occur in response to LPS. We hypothesize that in the absence of Ubqln1, mitochondrial depolarization leads to an accumulation of mitochondrial membrane proteins in the cytosol, which leads to translational inhibition and a cell cycle block. Overall design: For RNASeq, cells were stimulated in triplicate in 2*10e6 cells/mL for 4 hours with either 10 µg/mL anti-IgM F(ab)2 or 20 µg/mL LPS, or no stimulation. There were 18 total samples, 9 Knockout samples, 9 WT samples, 3 biological replicates per treatment group: no stimulation, 10 ug/mL a-Igm, 20 ug/mL LPS.
Publication Title
Ubiquilin1 promotes antigen-receptor mediated proliferation by eliminating mislocalized mitochondrial proteins.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We examined the transcriptional function of cyclin D1 in mouse development using two approaches. First, we queried association of cyclin D1 with the genome of E14.5 mouse embryos using ChIP-on-chip approach. We observed binding of cyclin D1 to several promoter regions. Second, we compared gene expression profiles between wild-type and cyclin D1-null retinas. We observed several transcripts with altered levels in cyclin D1-null organs.
Publication Title
Transcriptional role of cyclin D1 in development revealed by a genetic-proteomic screen.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 54 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
Molecular mechanisms underlying sarcopenia, the age-related loss of skeletal muscle mass and function, remain unclear. To identify molecular changes that correlated best with sarcopenia and might contribute to its pathogenesis, we determined global gene expression profiles in muscles of rats aged 6, 12, 18, 21, 24, and 27 months. These rats exhibit sarcopenia beginning at 21 months. Correlation of the gene expression versus muscle mass or age changes, and functional annotation analysis identified gene signatures of sarcopenia distinct from gene signatures of aging. Specifically, mitochondrial energy metabolism (e.g., tricarboxylic acid cycle and oxidative phosphorylation) pathway genes were the most downregulated and most significantly correlated with sarcopenia. Also, perturbed were genes/pathways associated with neuromuscular junction patency (providing molecular evidence of sarcopenia-related functional denervation and neuromuscular junction remodeling), protein degradation, and inflammation. Proteomic analysis of samples at 6, 18, and 27 months confirmed the depletion of mitochondrial energy metabolism proteins and neuromuscular junction proteins. Together, these findings suggest that therapeutic approaches that simultaneously stimulate mitochondrogenesis and reduce muscle proteolysis and inflammation have potential for treating sarcopenia.
Publication Title
Genomic and proteomic profiling reveals reduced mitochondrial function and disruption of the neuromuscular junction driving rat sarcopenia.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 20 Downloadable Samples
- IlluminaHiSeq2000
Description
Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. In addition, dysregulated proteins in the spinal cord of SOD1 mice that we identified in human ALS spinal cords and CSF were restored in SOD1G93A/miR155-/- mice. Treatment of SOD1 mice with anti-miR-155 SOD1 mice injected systemically or into the cerebrospinal fluid prolonged survival and restored the microglial unique genetic and microRNA profiles. Our findings provide a new avenue for immune based therapy of ALS by targeting miR-155. Overall design: Total RNA was isolated from whole lumbar spinal cord homogenate from healthy control donors without known neurologic diseases and sporadic and familial ALS.
Publication Title
Targeting miR-155 restores abnormal microglia and attenuates disease in SOD1 mice.
Sample Metadata Fields
No sample metadata fields
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