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Transcriptome profiling of Gastrocnemius from mice following supplementation with the combination of nicotinamide and pyridoxine (NAM/PN)

ABSTRACT: Transcriptome profiling of Gastrocnemius from mice following supplementation with the combination of nicotinamide and pyridoxine (NAM/PN)

PROVIDER: PRJNA1101866 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28732720.fastq.gz	Fastqsanger.gz
	SRR28732721.fastq.gz	Fastqsanger.gz
	SRR28732722.fastq.gz	Fastqsanger.gz
	SRR28732723.fastq.gz	Fastqsanger.gz
	SRR28732724.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of Gastrocnemius from mice following supplementation with the combination of nicotinamide and pyridoxine (NAM/PN)

Project description:Nicotinamide and pyridoxine have been identified in an in vitro screening as potent modulators of Muscel Stem cell activity. To test the in vivo efficacy (of NAM/PN) on muscle regneration, we used a mouse model of muscle injury and regeneration. Transcriptomic analyses on whole muscles harvested 5 days after muscle injury were performed to better understand the effect of NAM/PN.

2024-11-18 | GSE264284 | GEO

Transcriptome profiling of Muscle Stem cells from aged mice following treatment with the combination of nicotinamide (NAM) and pyridoxine (PN) for 3 days.

Project description:Nicotinamide and pyridoxine have been identified as potent modulators of Muscle Stem cell activity. We characterized genome-wide expression profiles of NAM/PN-treated MuSC and Vehicle to verify if NAM/PN supplementation reverses MuSC dysfunction during Aging.

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Transcriptome profiling of human myogenic progenitors following treatment with nicotinamide (NAM) or pyridoxine (PN) or the combination (NAM/PN).

Project description:Working with primary human myogenic progenitors (hMPs), we developed a high-content screen to discover molecules that enhanced myogenic function and identified NAM and PN as modulators of myogenic proliferation and differentiation. We characterized genome-wide expression profiles of NAM-, PN-treated and NAM/PN-treated hMPs with the goal to uncover the mechanisms of action of NAM and PN and the potential additivity from the combination at the molecular level in hMPs.

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Transcriptome profiling of human myogenic progenitors following treatment with nicotinamide (NAM) or pyridoxine (PN) or the combination (NAM/PN).

Project description:Transcriptome profiling of human myogenic progenitors following treatment with nicotinamide (NAM) or pyridoxine (PN) or the combination (NAM/PN).

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Transcriptome profiling of Muscle Stem cells from aged mice following treatment with the combination of nicotinamide (NAM) and pyridoxine (PN) for 3 days.

Project description:Transcriptome profiling of Muscle Stem cells from aged mice following treatment with the combination of nicotinamide (NAM) and pyridoxine (PN) for 3 days.

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Expression data for hiPSC-derived RPE treated with 10mM Nicotinamide or vehicle

Project description:We did the RNA-seq analysis to examine the global impact of Nicotinamide (NAM) on hiPSC-derived RPE transcriptome in order to better understand the mechanism of action of NAM. NAM inhibited the expression of Age related Macular degeneration (AMD) associated protein transcripts in hiPSC-derived RPE.

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Expression data for hiPSC-derived RPE treated with 10mM Nicotinamide or vehicle

Project description:Nicotinamide (NAM) inhibited the expression of Age related macular degeneration (AMD) associated proteins in hiPSC-derived retinal pigment epithelium (RPE). We did the microarray analysis to examine the global impact of NAM on hiPSC-derived RPE transcriptome in order to better understand the mechanism of action of NAM.

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Nicotinamide regulates LPS-induced HIF-1alpha responses through post-translational modifications in human macrophages

Project description:Mechanisms to control the immune response are important to pathogen evasion and host defense. Gram-negative bacteria are common pathogens that can activate host immune responses through their outer membrane component, lipopolysaccharide (LPS). Macrophages activated by LPS induce cell signals that promote hypoxic metabolism, phagocytosis, and antigen presentation. Nicotinamide (NAM) is a vitamin B3 derivative and precursor in the formation of nicotinamide adenine dinucleotide (NAD), which is a required co-factor in cellular function. In this study, treatment of human monocyte derived macrophages with NAM antagonized LPS-induced responses by altering the expression of ubiquitin genes, increasing HIF-1alpha and p65/RelA ubiquitination, decreasing p65/RelA acetylation and promoting the formation of the proteasome. NAM also elevated intracellular NAD levels and altered the genetic expression of sirtuins and poly(ADP-ribose) polymerases. These NAM responses highlight post-translational events in regulating the host response to pathogens and identify the ubiquitome as a target in pathogen evasion and host defense.

2023-05-01 | GSE188206 | GEO

Aged Mouse Muscle and Serum: Sedentary or Exercised Animals with or without Nicotinamide N-methyltransferase Inhibitor Treatment

Project description:Epigenomic profiling mouse gastrocnemius muscle and serum in aged female mice with/without exercise, with/without nicotinamide N-methyltransferase inhibitor treatment

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RNA-seq analyses for control and nicotinamide treated TNBC cells

Project description:In this study, we investigated how nicotinamide (NAM) affects cellular metabolism in TNBC cells and also such altered cellular metabolism by NAM is linked to cytotoxic functions through an integrated analysis of proteome and transcriptome data generated from three different TNBC cell lines, BT20, MB468, and MB231. By analyzing mRNA-seq data from control and NAM treated TNBC cells (3 replicates in each of 3 cell lines), we identified differentially expressed genes (DEGs), and associated cellular process. The up-regulated genes were associated with the processes related to cell death (programmed cell death, autophagy, and apoptotic mitochondrial changes) and mitochondria (organization, pH reduction/oxidation-reduction/NADP metabolism, response to starvation, respiratory chain, and lipid/oxoacid metabolism). On the other hand, the processes related to immune response (NF-kB and MAPK signaling, cell adhesion/migration, and response to cytokine) and cell proliferation were down-regulated consistently in the three TNBC cells.

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