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Liver tissue transcriptomic analysis of db/db mice expressing adenovirus-delivered GFP or NAMPT

ABSTRACT: Liver tissue transcriptomic analysis of db/db mice expressing adenovirus-delivered GFP or NAMPT

PROVIDER: PRJEB47703 | ENA |

REPOSITORIES: ENA

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Liver tissue transcriptomic analysis of db/db mice expressing adenovirus-delivered GFP or NAMPT

Project description:Hypothesis is that NAMPT overexpression alters liver transcriptomics in genetically diabetic, obese db/db mice. We treated db/db mice n = 4 with adenovirus encoding GFP or NAMPT by tail-vein delivery.

2022-08-01 | E-MTAB-10984 | biostudies-arrayexpress

Comparison of transcriptomic profile of the murine B16F1-GFP-M melanoma cells with the derived dormant B16F1-GFP-D, B16F1-GFP-DB#1, B16F1-GFP-DB#2, B16F1-GFP-DB#3 melanoma cells

Project description:Comparison of transcriptomic profile of the murine B16F1-GFP-M melanoma cells with the derived dormant B16F1-GFP-D, B16F1-GFP-DB#1, B16F1-GFP-DB#2, B16F1-GFP-DB#3 melanoma cells

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Comparison of transcriptomic profile of the murine B16F1-GFP-M melanoma cells with the derived dormant B16F1-GFP-D, B16F1-GFP-DB#1, B16F1-GFP-DB#2, B16F1-GFP-DB#3 melanoma cells

Project description:Cancer patients after successful therapy contain nested in their organs and/or circulating in the systemic fluids tumor cells that remain asymptomatic for an extended period of time. They stay dormant with no apparent immediate potential to develop into a clinically manifested tumor until activated by yet not well defined mechanisms. We previously developed tumor dormancy model of murine melanoma, a cancer with a high potential of phenotype plasticity to adapt to micro-environmental changes, in which to investigate cellular quiescence and related factors as a potential mechanism of tumour dormancy. In this study, to explore molecular mechanism responsible for cellular dormancy, we performed a comparative transcriptome analysis of dormant B16F1-GFP-D and derived dormant brain metastasis (DB) with maternal B16F1-GFP-M cells.

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Effect of systemic adipsin overexpression on db/db mouse pancreatic islets

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CD-1mice: db/db vs db/+

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The role of nicotinamide phosphoribosyltransferase (Nampt) in hippocampal neural stem/progenitor cells

Project description:Neural stem/progenitor cell (NSPC) proliferation and self-renewal, as well as insult-induced differentiation, decrease markedly with age, but the molecular mechanisms responsible for these declines remain unclear. Here we show that levels of NAD+ and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD+ biosynthesis, decrease with age in the hippocampus. Ablation of Nampt in adult NSPCs reduced their pool and proliferation in vivo. The decrease in the NSPC pool during aging can be rescued by enhancing hippocampal NAD+ levels. Nampt is the main source of NSPC NAD+ levels and required for G1/S progression of the NSPC cell cycle. Nampt is also critical for oligodendrocytic lineage fate decisions through a mechanism mediated redundantly by Sirt1 and Sirt2. Ablation of Nampt in the adult NSPCs in vivo reduced NSPC-mediated oligodendrogenesis upon injury. These phenotypes recapitulate defects in NSPCs during aging, implicating Nampt-mediated NAD+ biosynthesis as a mediator of these age-associated functional declines. Total RNA obtained from neurospheres derived from postnatal hippocampi subjected to 48 hours in vitro of incubation with Nampt-specific inhibitor FK866 (10 nM, 4 samples) or vehicle (DMSO, 1:1000, 4 samples).

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Profiling pancreatic islets from obese db/db and lean control db/+ mice

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Profiling pancreatic islets from obese db/db and lean control db/+ mice

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Anti-GCGR antibody treatment in db/db mice

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