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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)

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

PROVIDER: PRJNA1013933 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25939960_1.fastq.gz	Fastqsanger.gz
	SRR25939960_2.fastq.gz	Fastqsanger.gz
	SRR25939961_1.fastq.gz	Fastqsanger.gz
	SRR25939961_2.fastq.gz	Fastqsanger.gz
	SRR25939962_1.fastq.gz	Fastqsanger.gz

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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.

2023-09-07 | GSE242555 | GEO

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

Project description:Investigation of transcriptome changes in four human cell lines (BJ, BJ-5ta, U2OS and HeLa) after treatment for 24 hours with nicotinamide adenine dinucleotide (NAD+). Cells were untreated as the control condition. Nanopore sequencing of cDNA was performed after library preparation with the ONT SQK-PCB109 kit.

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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.

2022-02-25 | PXD022547 | Pride

Semisynthetic biosensors for mapping cellular concentrations of nicotinamide adenine dinucleotides.

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

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

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Project description:Mycobacteria can synthesize NAD+ using either the de novo biosynthesis pathway or the salvage pathway. The deletion of the three genes involved specifically in the NAD+ de novo biosynthesis pathway in the human pathogen Mycobacterium tuberculosis had no effect on the growth of the strain in vivo. In contrast, the same deletion in the bovine pathogen Mycobacterium bovis resulted in a strain that could not grow in vivo and could only grow in vitro with substantial nicotinamide supplmentation. This striking difference was attributed to the known defect in the nicotinamidase PncA of M. bovis, since introducing the M. tuberculosis pncA gene into the M. bovis strain defective for de novo NAD+ biosynthesis restored growth in vitro and in vivo. This study demonstrates that NAD+ starvation is a cidal event in mycobacteria and confirms that enzymes common to the de novo and salvage pathways may be good drug targets. We also propose that simultaneously targeting both the salvage and the de novo NAD+ biosynthesis pathways represents a potentially effective way to treat infection with tubercle bacilli. To characterize the lethality induced by nicotinamide starvation transcriptional profiling of the auxotrophs was performed. Triplicate 50 mL cultures of M. tuberculosis and M. bovis Delta nadABC mutants were grown in 7H9 OADC glycerol 0.05% tween broth in 500 mL roller bottles to an OD600nm= 0.1 in a roller incubator at 37Â°C. The cells were washed 1x in PBS and resuspended in 50 mL 7H9 OADC glycerol 0.05% tween broth with or without 20mg/L nicotinamide and returned to the incubator. After 7 days, cultures were harvested. Three biological replicates of each of two species with one dye-flip each

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Metabolism and biochemical properties of nicotinamide adenine dinucleotide (NAD) analogs, nicotinamide guanine dinucleotide (NGD) and nicotinamide hypoxanthine dinucleotide (NHD).

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