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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human ESCs differentiated in the presence or absence of nicotinamide

ABSTRACT: Human ESCs are pluripotent cells that have the capacity of self renewal for a prolonged period in vitro, and can differentiate into derivatives of all three primary germ layers: endoderm, mesoderm and ectoderm. Human ESCs are responsive to a wide range of factors in vitro that can direct their differentiation into specific cell types. We analyzed the effect of nicotinamide (NIC) on differentiation of hESCs in vitro. CEL file for GSM424319 is unavailable. Experiment Overall Design: hESCs were cultured as free-floating clusters in the presence of 10% FCS for 4 weeks in the presence or absence of nicotinamide.

ORGANISM(S): Homo sapiens

SUBMITTER: Temima Schnitzer Perlman

PROVIDER: E-GEOD-16919 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from hESCs differentiated in the presence or absence of nicotinamide

Project description:Human ESCs are pluripotent cells that have the capacity of self renewal for a prolonged period in vitro, and can differentiate into derivatives of all three primary germ layers: endoderm, mesoderm and ectoderm. Human ESCs are responsive to a wide range of factors in vitro that can direct their differentiation into specific cell types. We analyzed the effect of nicotinamide (NIC) on differentiation of hESCs in vitro. CEL file for GSM424319 is unavailable.

2009-10-02 | GSE16919 | GEO

ELAV proteomics after brain ischemia and reperfusion in the rat

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RNAseq evaluation of nicotinamide seed treatment analysed in Norway spruce seedlings

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2021-10-15 | E-MTAB-11007 | biostudies-arrayexpress

Nicotinamide Starvation of Mycobacteria Defective for de novo NAD Biosynthesis

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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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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Transcription of human thrombopoietin-induced megakaryocyte differentiation with and without nicotinamide vs. Universal reference sample

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The effect of nicotinamide on dysregulated genes associated with frataxin deficiency in FRDA.

Project description:To investigate the efficacy of nicotinamide treatment using our ex-vivo primary lymphocyte model, we performed high-throughput RNA sequencing on libraries generated from untreated and nicotinamide treated samples. PBMC isolated from FRDA affected individuals were cultured to prepare the primary lymphocyte cell lines. The primary cultured cells were either treated with 10mM nicotinamide or without the addition of drug during the 3-days treatment. RNA was extracted after the treatment and then RNA-seq libraries were generated by standard protocols.

2013-04-03 | E-GEOD-42960 | biostudies-arrayexpress

thrombopoietin-induced megakaryocyte differentiation with and without nicotinamide

2006-08-25 | GSE4974 | GEO

Nicotinamide promotes human pluripotent stem cells differentiation into cardiomyocytes [2]

Project description:Nicotinamide, the amide form of vitamin B3, is essential to maintain the human fetal development. It benefits the ectoderm and endoderm development, but its influence in mesoderm differentiation is elusive. In this study, we reported that nicotinamide regulated the gene expression of cardiovascular system, and it induced functional cardiomyocytes which was independent of canonical WNT signaling. Through a kinase screening, we found that nicotinamide inhibited the activity of P38δ to promote cardiomyocyte differentiation. Furthermore, we compared the gene expression of cardiomyocytes induced by WNT inhibitor IWP-2, nicotinamide or P38 inhibitor SB202190. The results showed that the cardiomyocytes induced by nicotinamide had similar gene expression profile compared with P38 inhibitor, which indicated nicotinamide promoted cardiac differentiation via the inhibition of P38.

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Nicotinamide promotes human pluripotent stem cells differentiation into cardiomyocytes [1]

2021-12-01 | GSE154453 | GEO

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