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Effect of NAMPT inhibition on gene expression in LPS/IFNg-stimulated primary mouse astrocytes

ABSTRACT: To investigate the role of NAMPT activity on astrocyte pro-inflmmatory activation

ORGANISM(S): Mus

PROVIDER: GSE205944 | GEO | 2022/08/12

REPOSITORIES: GEO

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Effect of depletion of CD38 on gene expression in LPS/IFNg-stimulated primary mouse astrocytes

Project description:To investigate the role of CD38 activity on astrocyte pro-inflmmatory activation

2022-08-12 | GSE205943 | GEO

RNA-sequencing of murine B16F10 melanoma cells with IFNg and FK866, a Nampt inhibitor

Project description:NAMPT is expressed in all cells during normal cell homeostasis. However, melanoma cells have a higher energetic demand and increase NAMPT expression. Our data show that IFNg signaling upregulates NAMPT in both human and mouse melanoma cells leading to increased cell growth and expression kinetics. The purpose of this experiment was to identify how IFNg inducible Nampt alters cell kinetics and we did this by treating melanoma cells with the combination of IFNg and FK866.

2023-07-01 | GSE207060 | GEO

Molecular sequelae of Nampt Inhibition in Human Multiple Myeloma cell line

Project description:Evaluation of specific coordinated pattern of transcriptional events consistent with anti-myeloma activity of FK866 (chemical Nampt inhibitor) 3 samples were analyzed using as control the untreated cells. Treated cells were cultured in presence of FK866 at concentration of 10nM for 6 and 24 hours.

2012-11-05 | E-GEOD-35414 | biostudies-arrayexpress

Molecular sequelae of Nampt Inhibition in Human Multiple Myeloma cell line

Project description:Evaluation of specific coordinated pattern of transcriptional events consistent with anti-myeloma activity of FK866 (chemical Nampt inhibitor)

2012-11-05 | GSE35414 | GEO

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).

2014-05-08 | E-GEOD-49784 | biostudies-arrayexpress

RNAi profiling of human MCF-7 cells depleted for NAMPT knockdown

Project description:NAMPT is an enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NAMPT knockdown on gene expression in MCF-7 breast cancer cells. Experiment Overall Design: Stable knockdown of NAMPT was achieved using a retroviral shRNA construct. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133 A2.0 microarrays.

2009-06-08 | E-GEOD-13449 | biostudies-arrayexpress

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

Expression analysis upon NAMPT knockdown in MCF-7 cells

2009-05-28 | GSE13449 | GEO

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

2014-05-08 | GSE49784 | GEO

NAMPT-dependent NAD+ biosynthesis controls circadian metabolism in a tissue-specific manner

Project description:Molecular clocks in the periphery coordinate tissue-specific daily biorhythms by integrating input from the hypothalamic master clock and intracellular metabolic signals. One such key metabolic signal is the cellular concentration of NAD+, which oscillates along with its biosynthetic enzyme, nicotinamide phosphoribosyltransferase (NAMPT). NAD+ levels feed back into the clock to influence rhythmicity of biological functions, yet whether this metabolic fine-tuning occurs ubiquitously across cell types and is a core clock feature is unknown. Here we show that NAMPT-dependent control over the molecular clock varies substantially between tissues. Brown adipose tissue (BAT) requires NAMPT to sustain the amplitude of the core clock, whereas rhythmicity in white adipose tissue (WAT) is only moderately dependent on NAD+ biosynthesis and the skeletal muscle clock is completely refractory to loss of NAMPT. In BAT and WAT, NAMPT differentially orchestrates oscillation of clock-controlled gene networks and the diurnality of metabolite levels. NAMPT coordinates the rhythmicity of TCA cycle intermediates in BAT, but not WAT, and loss of NAD+ abolishes these oscillations similarly to high fat diet (HFD)-induced circadian disruption. Adipose NAMPT depletion also improved the ability of animals to defend body temperature during cold stress but this is independent of time-of-day. Thus, our findings reveal that peripheral molecular clocks and metabolic biorhythms are shaped in a highly tissue-specific manner by NAMPT-dependent NAD+ synthesis.

2023-04-11 | GSE221550 | GEO

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