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Gene expression profile of brain tissue in wild-type and MSA Tg mice at the age of 24 weeks

ABSTRACT: Gene expression profile of brain tissue in wild-type and MSA Tg mice at the age of 24 weeks

PROVIDER: PRJNA862617 | ENA |

REPOSITORIES: ENA

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Gene expression profile of brain tissue in wild-type and MSA Tg mice at the age of 24 weeks

Project description:RNA was extracted from each brain of 3 WT and 3 Tg mice at the age of 24 weeks and pooled into one in each genotype group, and microarray analysis was performed.

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Gene expression profile of brain tissue in wild-type and MSA Tg mice at the age of 16 weeks

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Gene expression profile of brain tissue in wild-type and MSA Tg mice at the age of 16 weeks

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Expression data from liver of Retnla transgenic (Tg) and non-transgenic (non-Tg) mice.

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microRNA profiling by high-throughput sequencing in the substantia nigra and striatum of Multiple System Atrophy (MSA) transgenic mice and wild type controls

Project description:Multiple system atrophy (MSA) is a fatal rapidly progressive Ia-synucleinopathy, characterized by prominent Ia-synuclein accumulation in oligodendrocytes. In this study we investigated miRNA expression in the substantia nigra and striatum of MSA transgenic mice (Tg(Plp1-SNCA)1Haa) and wild type controls. This forms part of a larger study in which we investigated miRNA-mRNA regulatory network in substantia nigra and striatum of MSA transgenic mice in pre-motor stage of neurodegenration.

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Expression data from liver of Retnla transgenic (Tg) and non-transgenic (non-Tg) mice.

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Phosphoproteomic analysis of IL-2 MSA and IL-12 MSA combination on T cell signaling

Project description:Engineered cytokine-based approaches for immunotherapy of cancer are poised to enter the clinic, with IL-12 being at the forefront. However, little is known about potential mechanisms of resistance to cytokine therapies. We found that orthotopic murine lung tumors were resistant to systemically delivered IL-12 fused to murine serum albumin (MSA, IL12-MSA) due to low IL-12R expression on tumor-reactive CD8+ T cells. IL2-MSA increased binding of IL12-MSA by tumor-reactive CD8+ T cells, and combined administration of IL12-MSA and IL2-MSA led to enhanced tumor-reactive CD8+ T cell effector differentiation, decreased numbers of tumor-infiltrating CD4+ regulatory T (Treg) cells, and increased survival of lung tumor-bearing mice. Predictably, the combination of IL-2 and IL-12 at therapeutic doses led to significant dose-limiting toxicity. Administering IL-12 and IL-2 analogs with preferential binding to cells expressing IL12rb1 and CD25, respectively, led to a significant extension of survival in mice with lung tumors while abrogating dose-limiting toxicity. These findings suggest that IL-12 and IL-2 represent a rational approach to combination cytokine therapy whose dose-limiting toxicity can be overcome with engineered cytokine variants.

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