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PMID |
Sentence |
1 |
21152033
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Multiple roles for the non-coding RNA SRA in regulation of adipogenesis and insulin sensitivity.
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2 |
21152033
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Overexpression of SRA in ST2 mesenchymal precursor cells promotes their differentiation into adipocytes.
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3 |
21152033
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Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes involved in the cell cycle, and insulin and TNFα signaling pathways.
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4 |
21152033
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SRA in adipocytes increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin.
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5 |
21152033
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SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2.
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6 |
21152033
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SRA also inhibits the expression of adipocyte-related inflammatory genes and TNFα-induced phosphorylation of c-Jun NH(2)-terminal kinase.
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7 |
21152033
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In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways.
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8 |
23142275
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Cyclophosphamide (CY) in the dose of 175 mg/kg b.w. eliminated CD4+Foxp3+ regulatory T cells (Tregs) and enhanced disease severity in C57/BL6 mice, but it did not overcome resistance to diabetes in BALB/c mice and did not affect diabetes progression in ST2 knock-out (ST2KO) mice.
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9 |
23142275
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This treatment eliminated Tregs in pancreatic lymph nodes in ST2KO mice, while markedly increasing the influx of CD8+, CD4+TNF-α+, and CD4+IFN-γ+ effector T cells (Teffs) in pancreata.
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10 |
23142275
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Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3+ regulatory T cells in the pancreatic lymph nodes in diabetes modulation.
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11 |
23142275
|
Cyclophosphamide (CY) in the dose of 175 mg/kg b.w. eliminated CD4+Foxp3+ regulatory T cells (Tregs) and enhanced disease severity in C57/BL6 mice, but it did not overcome resistance to diabetes in BALB/c mice and did not affect diabetes progression in ST2 knock-out (ST2KO) mice.
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12 |
23142275
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This treatment eliminated Tregs in pancreatic lymph nodes in ST2KO mice, while markedly increasing the influx of CD8+, CD4+TNF-α+, and CD4+IFN-γ+ effector T cells (Teffs) in pancreata.
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13 |
23142275
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Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3+ regulatory T cells in the pancreatic lymph nodes in diabetes modulation.
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