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Nanopore RNA-seq of human cell lines treated with or without nicotinamide adenine dinucleotide (NAD+)

ABSTRACT: Nanopore RNA-seq of human cell lines treated with or without nicotinamide adenine dinucleotide (NAD+)

PROVIDER: PRJEB64552 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11758173.fastq.gz	Fastqsanger.gz
	ERR11758174.fastq.gz	Fastqsanger.gz
	ERR11758175.fastq.gz	Fastqsanger.gz
	ERR11758176.fastq.gz	Fastqsanger.gz
	ERR11758177.fastq.gz	Fastqsanger.gz

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Nanopore RNA-seq of human cell lines treated with or without nicotinamide adenine dinucleotide (NAD+)

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Reduced Nicotinamide Mononucleotide (NMNH) Potently Enhances NAD+, Suppresses Glycolysis and Cell Growth

Project description:In the present study, we developed a chemical method to produce dihydro nicotinamide mononucleotide (NMNH), which is the reduced-form of nicotinamide mononucleotide (NMN). We demonstrated that NMNH was a better nicotinamide adenine dinucleotide (NAD+) enhancer compared to NMN both in vitro and in vivo mediated by mononucleotide adenylyltransferase (NMNAT). Additionally, NMNH increased the reduced NAD (NADH) levels in cells and in mouse liver. Metabolomic analysis revealed that NMNH inhibited glycolysis and TCA cycle. In vitro experiments demonstrated that NMNH induced cell cycle arrest and suppressed cell growth. Nevertheless, NMNH treatment did not cause observable difference in mice. Taken together, our work demonstrates that NMNH is a potent NAD+ enhancer, and suppresses glycometabolism and cell growth.

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Project description:Doxorubicin (DOX) is the cornerstone of chemotherapy regimens for many malignancies, but its clinical usage is limited by severe cardiotoxicity. Accumulating evidence suggest that nicotinamide adenine dinucleotide (NAD+) depletion contributes to DOX-induced cardiotoxicity, making NAD+ boosting an appealing strategy. Nicotinamide mononucleotide (NMN) is an NAD+ precursor that shows promising therapeutic effects in various diseases. To understand the impact of NMN on gene expression in myocardial tissue of DOX-exposed mice, a RNA-seq assay was carried out.

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Illuminating the functions of understudied Fructosamine-3-kinase (FN3K) using a multi-omics approach reveals new links to nicotinamide adenine dinucleotides (NAD)

Project description:Fructosamine-3-kinases (FN3Ks) are a conserved family of repair enzymes that phosphorylate reactive sugars attached to lysine residues in peptides and proteins. Although FN3Ks are present across the tree of life and share detectable sequence similarity to eukaryotic protein kinases, the biological processes regulated by these kinases are largely unknown. To address this knowledge gap, we leveraged the FN3K CRISPR Knock-Out (KO) cell line alongside an integrative multi-omics study combining transcriptomics, interactomics, metabolomics, and genomics to place these enzymes in a pathway context. The integrative analyses revealed the enrichment of pathways related to oxidative stress response, lipid biosynthesis (cholesterol and fatty acids), carbon and co-factor metabolism, and protein translational machinery. Moreover, statistically significant enrichment of metallothioneins and nicotinamide adenine dinucleotide (NAD) binding proteins suggest potential links between FN3Ks and NAD-mediated energy metabolism and redox balance. We report specific binding of human FN3K to NAD compounds in a metal and concentration-dependent manner and provide insight into their binding mode using modeling and experimental site-directed mutagenesis. By identifying a potential link between FN3Ks, redox regulation, and NAD-dependent metabolic processes, our studies provide a framework for targeting these understudied kinases in diabetic complications and other metabolic disorders.

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Nicotinamide riboside augments the human skeletal muscle NAD+ 1 metabolome and induces transcriptomic and anti-inflammatory signatures in aged subjects: a placebo-controlled, randomized trial

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