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Nmnat

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https://www.readbyqxmd.com/read/29748257/metabolic-regulation-of-transcription-through-compartmentalized-nad-biosynthesis
#1
Keun Woo Ryu, Tulip Nandu, Jiyeon Kim, Sridevi Challa, Ralph J DeBerardinis, W Lee Kraus
NAD+ (nicotinamide adenine dinucleotide in its oxidized state) is an essential molecule for a variety of physiological processes. It is synthesized in distinct subcellular compartments by three different synthases (NMNAT-1, -2, and -3). We found that compartmentalized NAD+ synthesis by NMNATs integrates glucose metabolism and adipogenic transcription during adipocyte differentiation. Adipogenic signaling rapidly induces cytoplasmic NMNAT-2, which competes with nuclear NMNAT-1 for the common substrate, nicotinamide mononucleotide, leading to a precipitous reduction in nuclear NAD+ levels...
May 11, 2018: Science
https://www.readbyqxmd.com/read/29727704/overexpression-of-nmnat-improves-the-adaption-of-health-span-in-aging-drosophila
#2
Xianchu Liu, Zhuo Xiang, Qiufang Li, Xiangcheng Ruan, Kaixin Xiong, Wen Dengtai, Lan Zheng
Nmnat is a stress response protein which has been involved in a variety of biological processes. However, the effects of Nmnat on aging have not yet been investigated. The present study revealed the effects of Nmnat on aging of Drosophila and uncovered its underlying mechanism. Therefore, the overexpression of Nmnat was established by arm/Gal4 system in Drosophila with an aim to determine the functions of Nmnat during aging process. In this study, our results showed Nmnat was a positive factor on lifespan and movement capacity, which was consistent on d-galactose induced aging acceleration...
May 1, 2018: Experimental Gerontology
https://www.readbyqxmd.com/read/29716954/nmnat-mitigates-sensory-dysfunction-in-a-drosophila-model-of-paclitaxel-induced-peripheral-neuropathy
#3
Jennifer M Brazill, Beverley Cruz, Yi Zhu, R Grace Zhai
Chemotherapy-induced peripheral neuropathy (CIPN) is the major dose-limiting side effect of many commonly used chemotherapeutic agents, including paclitaxel. Currently there are no neuroprotective or effective symptomatic treatments for CIPN. Lack of understanding of the in vivo mechanisms of CIPN has greatly impeded the identification of therapeutic targets. Here we optimized a model of paclitaxel-induced peripheral neuropathy using Drosophila larvae that recapitulates aspects of chemotherapy-induced sensory dysfunction ...
April 30, 2018: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/29642910/localization-and-phosphorylation-of-plasmodium-falciparum-nicotinamide-nicotinate-mononucleotide-adenylyltransferase-pfnmnat-in-intraerythrocytic-stages
#4
Carlos A Nieto, Lina M Sánchez, Diana M Sánchez, Gonzalo J Díaz, María H Ramírez
BACKGROUND: Nicotinamide adenine dinucleotide (NAD+) is an essential molecule in the energy metabolism of living beings, and it has various cellular functions. The main enzyme in the biosynthesis of this nucleotide is nicotinamide/nicotinate mononucleotide adenylyltransferase (NMNAT, EC 2.7.7.1/18) because it is the convergence point for all known biosynthetic pathways. NMNATs have divergences in both the number of isoforms detected and their distribution, depending on the organism. METHODS: In the laboratory of basic research in biochemistry (LIBBIQ: acronym in Spanish) the NMNATs of protozoan parasites (Leishmania braziliensis, Plasmodium falciparum, Trypanosoma cruzi, and Giardia duodenalis) have been studied, analysing their catalytic properties through the use of proteins...
April 11, 2018: Malaria Journal
https://www.readbyqxmd.com/read/29478906/identification-of-the-nicotinamide-salvage-pathway-as-a-new-toxification-route-for-antimetabolites
#5
Daniela Buonvicino, Francesca Mazzola, Federica Zamporlini, Francesco Resta, Giuseppe Ranieri, Emidio Camaioni, Mirko Muzzi, Riccardo Zecchi, Giuseppe Pieraccini, Christian Dölle, Massimo Calamante, Gianluca Bartolucci, Mathias Ziegler, Barbara Stecca, Nadia Raffaelli, Alberto Chiarugi
Interest in the modulation of nicotinamide adenine dinucleotide (NAD) metabolome is gaining great momentum because of its therapeutic potential in different human disorders. Suppression of nicotinamide salvage by nicotinamide phosphoribosyl transferase (NAMPT) inhibitors, however, gave inconclusive results in neoplastic patients because several metabolic routes circumvent the enzymatic block converging directly on nicotinamide mononucleotide adenylyl transferases (NMNATs) for NAD synthesis. Unfortunately, NMNAT inhibitors have not been identified...
April 19, 2018: Cell Chemical Biology
https://www.readbyqxmd.com/read/29175372/nad-biosynthetic-enzyme-nmnat1-reduces-early-behavioral-impairment-in-the-htau-mouse-model-of-tauopathy
#6
Francesca Rossi, Philippine C Geiszler, Weina Meng, Matthew R Barron, Malcolm Prior, Anna Herd-Smith, Andrea Loreto, Maria Yanez Lopez, Henryk Faas, Marie-Christine Pardon, Laura Conforti
NAD metabolism and the NAD biosynthetic enzymes nicotinamide nucleotide adenylyltransferases (NMNATs) are thought to play a key neuroprotective role in tauopathies, including Alzheimer's disease. Here, we investigated whether modulating the expression of the NMNAT nuclear isoform NMNAT1, which is important for neuronal maintenance, influences the development of behavioral and neuropathological abnormalities in htau mice, which express non-mutant human tau isoforms and represent a model of tauopathy relevant to Alzheimer's disease...
February 26, 2018: Behavioural Brain Research
https://www.readbyqxmd.com/read/29175123/characterization-and-application-of-a-novel-nicotinamide-mononucleotide-adenylyltransferase-from-thermus-thermophilus-hb8
#7
Kenji Konishi, Shigeru Ueda, Miki Kawano, Susumu Osawa, Tomohiro Tamura, Eisaku Hokazono, Yuzo Kayamori, Shin-Ichi Sakasegawa
Herein, we describe a novel enzymatic cycling method to measure nicotinamide mononucleotide (NMN) or nicotinic acid mononucleotide (NaMN), which are precursors of NAD biosynthesis. A gene encoding an NMN adenylyltransferase (NMNAT, EC 2.7.7.1) homologue was identified in Thermus thermophilus HB8. The gene from T. thermophilus (TtNMNAT) was engineered for expression in Escherichia coli and the recombinant enzyme found to be stable, retaining full activity after incubation for 45 min at 70°C. The Km values for NMN and ATP were calculated to be 0...
November 23, 2017: Journal of Bioscience and Bioengineering
https://www.readbyqxmd.com/read/29046881/nmnat3-is-protective-against-the-effects-of-neonatal-cerebral-hypoxia-ischemia
#8
Rafael Galindo, Marianne Banks Greenberg, Toshiyuki Araki, Yo Sasaki, Nehali Mehta, Jeffrey Milbrandt, David M Holtzman
OBJECTIVE: To determine whether the NAD+ biosynthetic protein, nicotinamide mononucleotide adenylyltransferase-3 (NMNAT3), is a neuroprotective inducible enzyme capable of decreasing cerebral injury after neonatal hypoxia-ischemia (H-I) and reducing glutamate receptor-mediated excitotoxic neurodegeneration of immature neurons. METHODS: Using NMNAT3-overexpressing mice we investigated whether increases in brain NMNAT3 reduced cerebral tissue loss following H-I. We then employed biochemical methods from injured neonatal brains to examine the inducibility of NMNAT3 and the mechanism of NMNAT3-dependent neuroprotection...
October 2017: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/29029387/the-%C3%AE-nad-salvage-pathway-and-pkc-mediated-signaling-influence-localized-parp-1-activity-and-ctcf-poly-adp-ribosylation
#9
David J P Henderson, Jj L Miranda, Beverly M Emerson
Poly(ADP)ribosylation (PARylation) of the chromatin architectural protein CTCF is critical for CTCF-dependent regulation of chromatin boundary and insulator elements. Loss of CTCF PARylation results in epigenetic silencing of certain tumor suppressor genes through destabilization of nearby chromatin boundaries. We investigated the metabolic and mechanistic processes that regulate PARP-1-mediated CTCF PARylation in human cancer cell lines and discovered a key role for the expression and activity of β-NAD+ salvage enzymes, NAMPT and NMNAT-1...
September 12, 2017: Oncotarget
https://www.readbyqxmd.com/read/28743869/nicotinamide-mononucleotide-and-related-metabolites-induce-disease-resistance-against-fungal-phytopathogens-in-arabidopsis-and-barley
#10
Akihiro Miwa, Yuji Sawada, Daisuke Tamaoki, Masami Yokota Hirai, Makoto Kimura, Kazuhiro Sato, Takumi Nishiuchi
Nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide (NAD), is known to act as a functional molecule in animals, whereas its function in plants is largely unknown. In this study, we found that NMN accumulated in barley cultivars resistant to phytopathogenic fungal Fusarium species. Although NMN does not possess antifungal activity, pretreatment with NMN and related metabolites enhanced disease resistance to Fusarium graminearum in Arabidopsis leaves and flowers and in barley spikes...
July 25, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28683272/axon-death-pathways-converge-on-axundead-to-promote-functional-and-structural-axon-disassembly
#11
Lukas J Neukomm, Thomas C Burdett, Andrew M Seeds, Stefanie Hampel, Jaeda C Coutinho-Budd, Jonathan E Farley, Jack Wong, Yonca B Karadeniz, Jeannette M Osterloh, Amy E Sheehan, Marc R Freeman
Axon degeneration is a hallmark of neurodegenerative disease and neural injury. Axotomy activates an intrinsic pro-degenerative axon death signaling cascade involving loss of the NAD(+) biosynthetic enzyme Nmnat/Nmnat2 in axons, activation of dSarm/Sarm1, and subsequent Sarm-dependent depletion of NAD(+). Here we identify Axundead (Axed) as a mediator of axon death. axed mutants suppress axon death in several types of axons for the lifespan of the fly and block the pro-degenerative effects of activated dSarm in vivo...
July 5, 2017: Neuron
https://www.readbyqxmd.com/read/28671679/2-deoxyadenosine-5-diphosphoribose-is-an-endogenous-trpm2-superagonist
#12
Ralf Fliegert, Andreas Bauche, Adriana-Michelle Wolf Pérez, Joanna M Watt, Monika D Rozewitz, Riekje Winzer, Mareike Janus, Feng Gu, Annette Rosche, Angelika Harneit, Marianne Flato, Christelle Moreau, Tanja Kirchberger, Valerie Wolters, Barry V L Potter, Andreas H Guse
Transient receptor potential melastatin 2 (TRPM2) is a ligand-gated Ca2+ -permeable nonselective cation channel. Whereas physiological stimuli, such as chemotactic agents, evoke controlled Ca2+ signals via TRPM2, pathophysiological stimuli such as reactive oxygen species and genotoxic stress result in prolonged TRPM2-mediated Ca2+ entry and, consequently, apoptosis. To date, adenosine 5'-diphosphoribose (ADPR) has been assumed to be the main agonist for TRPM2. Here we show that 2'-deoxy-ADPR was a significantly better TRPM2 agonist, inducing 10...
September 2017: Nature Chemical Biology
https://www.readbyqxmd.com/read/28445802/nmnat-it-s-an-nad-synthase%C3%A2-it-s-a-chaperone%C3%A2-it-s-a-neuroprotector
#13
REVIEW
Jennifer M Brazill, Chong Li, Yi Zhu, R Grace Zhai
Nicotinamide mononucleotide adenylyl transferases (NMNATs) are a family of highly conserved proteins indispensable for cellular homeostasis. NMNATs are classically known for their enzymatic function of catalyzing NAD+ synthesis, but also have gained a reputation as essential neuronal maintenance factors. NMNAT deficiency has been associated with various human diseases with pronounced consequences on neural tissues, underscoring the importance of the neuronal maintenance and protective roles of these proteins...
June 2017: Current Opinion in Genetics & Development
https://www.readbyqxmd.com/read/28293166/protein-remodeling-factors-as-potential-therapeutics-for-neurodegenerative-disease
#14
REVIEW
Meredith E Jackrel, James Shorter
Protein misfolding is implicated in numerous neurodegenerative disorders including amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, and Huntington's disease. A unifying feature of patients with these disorders is the accumulation of deposits comprised of misfolded protein. Aberrant protein folding can cause toxicity through a loss or gain of protein function, or both. An intriguing therapeutic approach to counter these disorders is the application of protein-remodeling factors to resolve these misfolded conformers and return the proteins to their native fold and function...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28262487/nmn-deamidase-delays-wallerian-degeneration-and-rescues-axonal-defects-caused-by-nmnat2-deficiency-in%C3%A2-vivo
#15
Michele Di Stefano, Andrea Loreto, Giuseppe Orsomando, Valerio Mori, Federica Zamporlini, Richard P Hulse, Jamie Webster, Lucy F Donaldson, Martin Gering, Nadia Raffaelli, Michael P Coleman, Jonathan Gilley, Laura Conforti
Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive. Injury or genetically induced depletion of NMNAT2 triggers axonal degeneration or defective axon growth. We have previously proposed that axonal NMNAT2 primarily promotes axon survival by maintaining low levels of its substrate NMN rather than generating NAD; however, this is still debated. NMN deamidase, a bacterial enzyme, shares NMN-consuming activity with NMNAT2, but not NAD-synthesizing activity, and it delays axon degeneration in primary neuronal cultures...
March 20, 2017: Current Biology: CB
https://www.readbyqxmd.com/read/27923046/mitochondria-and-caspases-tune-nmnat-mediated-stabilization-to-promote-axon-regeneration
#16
Li Chen, Derek M Nye, Michelle C Stone, Alexis T Weiner, Kyle W Gheres, Xin Xiong, Catherine A Collins, Melissa M Rolls
Axon injury can lead to several cell survival responses including increased stability and axon regeneration. Using an accessible Drosophila model system, we investigated the regulation of injury responses and their relationship. Axon injury stabilizes the rest of the cell, including the entire dendrite arbor. After axon injury we found mitochondrial fission in dendrites was upregulated, and that reducing fission increased stabilization or neuroprotection (NP). Thus axon injury seems to both turn on NP, but also dampen it by activating mitochondrial fission...
December 2016: PLoS Genetics
https://www.readbyqxmd.com/read/27817743/new-insights-into-the-roles-of-nad-poly-adp-ribose-metabolism-and-poly-adp-ribose-glycohydrolase
#17
REVIEW
Seiichi Tanuma, Akira Sato, Takahiro Oyama, Atsushi Yoshimori, Hideaki Abe, Fumiaki Uchiumi
Accumulating evidence has suggested the fundamental functions of NAD+-poly(ADP-ribose) metabolism in cellular and physiological processes, including energy homeostasis, signal transduction, DNA transaction, genomic stability and cell death or survival. The NAD+ biosynthesis and poly(ADP-ribose) [(ADP-R)n] turnover are tightly controlled by several key enzymes, such as nicotinamide phosphoribosyltransferase (NmPRT), nicotinamide mononucleotide adenylyltransferases (NMNATs), poly(ADP-ribose) polymerase (PARP), poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribose pyrophosphorylase (ADPRPPL)...
2016: Current Protein & Peptide Science
https://www.readbyqxmd.com/read/27783719/nicotinamide-mononucleotide-adenylyltransferase-of-trypanosoma-cruzi-tcnmnat-a-cytosol-protein-target-for-serine-kinases
#18
Diana Milena Sánchez-Lancheros, Luis Fernando Ospina-Giraldo, María Helena Ramírez-Hernández
Nicotinamide/nicotinate adenine dinucleotide (NAD+/NaAD) performs essential functions in cell metabolism and energy production due to its redox properties. The nicotinamide/nicotinate mononucleotide adenylyltransferase (NMNAT, EC 2.7.7.1/18) enzyme catalyses the key step in the biosynthesis of NAD+. Previously, the enzyme NMNAT was identified in Trypanosoma cruzi (TcNMNAT), a pathogenic agent with epidemiological importance in Latin America. To continue with the functional characterisation of this enzyme, its subcellular location and its possible post-translational modifications were examined in this study...
November 2016: Memórias do Instituto Oswaldo Cruz
https://www.readbyqxmd.com/read/27547771/nmnat1-protects-neuronal-function-without-altering-phospho-tau-pathology-in-a-mouse-model-of-tauopathy
#19
Erik S Musiek, David D Xiong, Tirth Patel, Yo Sasaki, Yinong Wang, Adam Q Bauer, Risham Singh, Samantha L Finn, Joseph P Culver, Jeffrey Milbrandt, David M Holtzman
OBJECTIVE: The nicotinamide-nucleotide adenylyltransferase protein Nmnat1 is a potent inhibitor of axonal degeneration in models of acute axonal injury. Hyperphosphorylation and aggregation of the microtubule-associated protein Tau are associated with neurodegeneration in Alzheimer's Disease and other disorders. Previous studies have demonstrated that other Nmnat isoforms can act both as axonoprotective agents and have protein chaperone function, exerting protective effects in drosophila and mouse models of tauopathy...
June 2016: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/27425894/nicotinamide-mononucleotide-inhibits-post-ischemic-nad-degradation-and-dramatically-ameliorates-brain-damage-following-global-cerebral-ischemia
#20
Ji H Park, Aaron Long, Katrina Owens, Tibor Kristian
Nicotinamide adenine dinucleotide (NAD(+)) is an essential cofactor for multiple cellular metabolic reactions and has a central role in energy production. Brain ischemia depletes NAD(+) pools leading to bioenergetics failure and cell death. Nicotinamide mononucleotide (NMN) is utilized by the NAD(+) salvage pathway enzyme, nicotinamide adenylyltransferase (Nmnat) to generate NAD(+). Therefore, we examined whether NMN could protect against ischemic brain damage. Mice were subjected to transient forebrain ischemia and treated with NMN or vehicle at the start of reperfusion or 30min after the ischemic insult...
November 2016: Neurobiology of Disease
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