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ATP + 1-(beta-D-ribofuranosyl)-nicotinamide = ADP + beta-nicotinamide D-ribonucleotide
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide = ADP + beta-nicotinamide D-ribonucleotide
enzyme has both ribosylnicotinamide kinase, i.e. EC 2.7.1.22, and nicotinamide mononucleotide adenylyltransferase, i.e. EC 2.7.7.18, activity
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ATP + 1-(beta-D-ribofuranosyl)-nicotinamide = ADP + beta-nicotinamide D-ribonucleotide
enzyme has both ribosylnicotinamide kinase, i.e. EC 2.7.1.22, and nicotinamide mononucleotide adenylyltransferase, i.e. EC 2.7.7.18, activity
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ATP + 1-(beta-D-ribofuranosyl)-nicotinamide = ADP + beta-nicotinamide D-ribonucleotide
enzyme has both ribosylnicotinamide kinase, i.e. EC 2.7.1.22, and nicotinamide mononucleotide adenylyltransferase, i.e. EC 2.7.7.18, activity
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide = ADP + beta-nicotinamide D-ribonucleotide
bifunctional enzyme exhibiting nicotinamide ribose kinase activity, EC 2.7.1.22, and weak adenylyltransferase activity, EC 2.7.7.1
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ATP + 1-(beta-D-ribofuranosyl)-nicotinamide = ADP + beta-nicotinamide D-ribonucleotide
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ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
ATP + nicotinamide mononucleotide
NAD+ + diphosphate
GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
GDP + beta-nicotinamide D-ribonucleotide
phosphate + inosine
?
-
-
-
-
?
phosphate + nicotinamide riboside
nicotinamide + ribose-1-phosphate
-
-
-
r
additional information
?
-
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
involved in NAD salvage pathway
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
no activity with N-ribosylnicotinate
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
involved in NAD salvage pathway
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
nicotinamide riboside phosphorylation step is essential for both nicotinamide riboside uptake across the inner membrane and NAD+ synthesis and is also involved in controlling the NAD+ biosynthesis rate
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
-
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
involved in NAD salvage pathway
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
activity is essential for N-ribosylnicotinamide assimilation
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
-
-
?
ATP + nicotinamide mononucleotide
NAD+ + diphosphate
-
-
-
r
ATP + nicotinamide mononucleotide
NAD+ + diphosphate
-
-
r
ATP + nicotinamide mononucleotide
NAD+ + diphosphate
-
-
-
r
GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
GDP + beta-nicotinamide D-ribonucleotide
-
-
-
?
GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
GDP + beta-nicotinamide D-ribonucleotide
-
-
-
?
additional information
?
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enzyme NRK2 highly prefers ATP, while isozyme NRK1 also uses GTP with similar activity
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-
additional information
?
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enzyme NRK2 highly prefers ATP, while isozyme NRK1 also uses GTP with similar activity
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-
additional information
?
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enzyme NRK2 is restricted to ATP, while isozyme NRK1 also uses GTP
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-
-
additional information
?
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enzyme NRK2 is restricted to ATP, while isozyme NRK1 also uses GTP
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-
-
additional information
?
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-
the enzymes' C-terminal domain has nicotinamide ribose kinase activity, the central domain performes adenylyltransferase reaction, EC 2.7.7.1, overview, the purified enzyme binds nadB promotor sequence in absence of ATP with or without NAD+, DNA binding activity of the enzyme is regulated by ATP binding to the adenylyltransferase domain
-
-
?
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ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
GDP + beta-nicotinamide D-ribonucleotide
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
ADP + beta-nicotinamide D-ribonucleotide
-
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
involved in NAD salvage pathway
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
involved in NAD salvage pathway
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
nicotinamide riboside phosphorylation step is essential for both nicotinamide riboside uptake across the inner membrane and NAD+ synthesis and is also involved in controlling the NAD+ biosynthesis rate
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+
-
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
involved in NAD salvage pathway
-
?
ATP + N-ribosylnicotinamide
ADP + nicotinamide ribonucleotide
-
activity is essential for N-ribosylnicotinamide assimilation
-
-
?
GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
GDP + beta-nicotinamide D-ribonucleotide
-
-
-
?
GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
GDP + beta-nicotinamide D-ribonucleotide
-
-
-
?
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malfunction
loss of NRK-2 enhances p38alpha activation following ischemic injury
malfunction
nicotinamide riboside kinase 2 (NRK2) deficiency alone has minimal impact in wild-type mice
malfunction
NRK-2 plays a critical role in heart failure progression following ischemic injury. NRK-2 deficiency promotes post-MI scar expansion, rapid LV chamber dilatation, cardiac dysfunction and fibrosis possibly due to increased p38slphs activation
malfunction
NRK1 deficiency leads to decreased gluconeogenic potential and impaired mitochondrial function. Upon high-fat feeding, NRK1 deficient mice develop glucose intolerance, insulin resistance and hepatosteatosis. They are more susceptible to diet-induced liver DNA damage, due to compromised PARP1 activity
malfunction
NRK1, NRK2, and double KO myotubes reveal redundancy in the nicotinamide riboside kinase dependent metabolism of nicotinamide riboside to NAD+
malfunction
Nrk2 knockout mice develop normally and show subtle alterations to their NAD+ metabolome and expression of related genes. NRK1, NRK2, and double KO myotubes reveal redundancy in the nicotinamide riboside kinase dependent metabolism of nicotinamide riboside to NAD+
malfunction
a murine NRK1 loss-of-function model does not exhibit any gross phenotypic abnormalities, with steady state NAD+ levels unaffected, at least in the tissues that are examined (liver, skeletal muscle, brown adipose and kidney)
malfunction
a murine NRK2 loss-of-function model does not exhibit any gross phenotypic abnormalities, with steady state NAD+ levels unaffected, at least in the tissues that are examined (liver, skeletal muscle, brown adipose and kidney)
malfunction
induction of the nicotinamide riboside kinase NAD+ salvage pathway in a model of sarcoplasmic reticulum dysfunction. hexose-6-phosphate dehydrogenase (H6PD)-KO skeletal muscle shows adaptations in the routes regulating nicotinamide and NAD+ biosynthesis, with significant activation of the nicotinamide riboside kinase 2 (NRK2) pathway. Associated with changes in NAD+ biosynthesis, H6PD-KO muscle has impaired mitochondrial respiratory capacity with altered mitochondrial acylcarnitine and acetyl-CoA metabolism. Boosting NAD+ levels through the NRK2 pathway using the precursor nicotinamide riboside elevated NAD+/NADH but has no effect to mitigate endoplasmic reticulum stress and dysfunctional mitochondrial respiratory capacity or acetyl-CoA metabolism. Similarly, H6PD-KO/NRK2 double KO mice do not display an exaggerated timing or severity of myopathy or overt change in mitochondrial metabolism despite depression of NAD+ availability. H6PDKO/NRK2 double KO mice do not display an exaggerated timing or severity of myopathy or overt change in mitochondrial metabolism despite depression of NAD+ availability. Alterations in nicotinamide metabolism in H6PD-KO muscle, overview. Upregulation of NRK2 may be an early adaptive response to metabolic stress and the need to defend NAD+ availability
malfunction
loss of NRK-2 enhanced p38alpha activation following ischemic injury. The gain of NRK-2 function suppresses the p38alpha as well as fibroblast activation (alpha-SMA expression) upon TGF-beta stimulation, and limits cardiomyocytes death upon hypoxia/re-oxygenation. Role of NRK-2 in ischemia-induced cardiac remodeling and dysfunction, overview
malfunction
-
nicotinamide riboside kinase 2 (NRK2) deficiency alone has minimal impact in wild-type mice
-
malfunction
-
induction of the nicotinamide riboside kinase NAD+ salvage pathway in a model of sarcoplasmic reticulum dysfunction. hexose-6-phosphate dehydrogenase (H6PD)-KO skeletal muscle shows adaptations in the routes regulating nicotinamide and NAD+ biosynthesis, with significant activation of the nicotinamide riboside kinase 2 (NRK2) pathway. Associated with changes in NAD+ biosynthesis, H6PD-KO muscle has impaired mitochondrial respiratory capacity with altered mitochondrial acylcarnitine and acetyl-CoA metabolism. Boosting NAD+ levels through the NRK2 pathway using the precursor nicotinamide riboside elevated NAD+/NADH but has no effect to mitigate endoplasmic reticulum stress and dysfunctional mitochondrial respiratory capacity or acetyl-CoA metabolism. Similarly, H6PD-KO/NRK2 double KO mice do not display an exaggerated timing or severity of myopathy or overt change in mitochondrial metabolism despite depression of NAD+ availability. H6PDKO/NRK2 double KO mice do not display an exaggerated timing or severity of myopathy or overt change in mitochondrial metabolism despite depression of NAD+ availability. Alterations in nicotinamide metabolism in H6PD-KO muscle, overview. Upregulation of NRK2 may be an early adaptive response to metabolic stress and the need to defend NAD+ availability
-
malfunction
-
loss of NRK-2 enhances p38alpha activation following ischemic injury
-
malfunction
-
loss of NRK-2 enhanced p38alpha activation following ischemic injury. The gain of NRK-2 function suppresses the p38alpha as well as fibroblast activation (alpha-SMA expression) upon TGF-beta stimulation, and limits cardiomyocytes death upon hypoxia/re-oxygenation. Role of NRK-2 in ischemia-induced cardiac remodeling and dysfunction, overview
-
metabolism
metabolome analysis. Upregulation of NRK2 may be an early adaptive response to metabolic stress and the need to defend NAD+ availability
metabolism
the enzyme is involved in the NAD+ biosynthesis pathway. In the initial step of the pathway, NRK activity catalyses the phosphorylation of nicotinamide riboside (NR) to nicotinamide mononucleotide (NMN). Importance of different salvage pathways involved in metabolising the vitamin B3 class of NAD+ precursor molecules, with a particular focus on the nicotinamide riboside kinase pathway at both a tissue-specific and systemic level, overview
metabolism
the enzyme is involved in the NAD+ biosynthesis pathway. In the initial step of the pathway, NRK activity catalyses the phosphorylation of nicotinamide riboside (NR) to nicotinamide mononucleotide (NMN). Importance of different salvage pathways involved in metabolising the vitamin B3 class of NAD+ precursor molecules, with a particular focus on the nicotinamide riboside kinase pathway at both a tissue-specific and systemic level, regulation of the NRK enzymes, overview. Alternatively, NRK activity can phosphorylate nicotinic acid riboside (NaR) to nicotinic acid mononucleotide (NaMN), see for EC 2.7.1.173
metabolism
the enzyme is involved in the NAD+ biosynthesis pathway. In the initial step of the pathway, NRK activity catalyses the phosphorylation of nicotinamide riboside (NR) to nicotinamide mononucleotide (NMN). Importance of different salvage pathways involved in metabolising the vitamin B3 class of NAD+ precursor molecules, with a particular focus on the nicotinamide riboside kinase pathway at both a tissue-specific and systemic level, regulation of the NRK enzymes, overview. Alternatively, NRK activity can phosphorylate nicotinic acid riboside (NaR) to nicotinic acid mononucleotide (NaMN), see for EC 2.7.1.173
metabolism
-
metabolome analysis. Upregulation of NRK2 may be an early adaptive response to metabolic stress and the need to defend NAD+ availability
-
physiological function
NRK-2 plays a critical role in heart failure progression following ischemic injury. NRK-2 deficiency promotes post-MI scar expansion, rapid LV chamber dilatation, cardiac dysfunction and fibrosis possibly due to increased p38slphs activation
physiological function
NRK1 and 2 display overlapping function in salvage of exogenous nicotinamide riboside and NMN to augment intracellular NAD+ availability
physiological function
-
the enzyme is necessary and rate-limiting for the use of exogenous nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) for NAD+ synthesis. The role of NRK1 in driving NAD+ synthesis from other NAD+ precursors, such as nicotinamide or nicotinic acid, is dispensable
physiological function
the enzyme is nrate-limiting and essential for nicotinamide riboside-induced NAD+ synthesis in hepatic cells
physiological function
upregulation of nicotinamide riboside kinase 2 (NRK2) mediated salvage of nicotinamide riboside into NAD+ is an early adaptation to perturbed muscle sarcoplasmic reticulum NAD(P)(H) homeostasis and impaired mitochondrial energy production in hexose-6-posphate dehydrogenase deficiency
physiological function
although NRK1 and NRK2 do not appear critical in mice for endogenous NR salvage to NAD+, their activity has been determined essential for the utilisation of exogenous NR and, more surprisingly, NMN. Without expression of the NRK enzymes in tissues, the NAD+-boosting effects of nicotinamide riboside (NR) and NMN supplementation is blocked, whilst expression of alternative NAD+ biosynthesis enzymes remains comparable to wild-type mice. Phosphorylation of NR by NRK1 appears preferred to NRK2 even in skeletal muscle where Nmrk2 is specifically expressed and found at substantially higher mRNA levels than Nmrk1
physiological function
although NRK1 and NRK2 do not appear critical in mice for endogenous NR salvage to NAD+, their activity has been determined essential for the utilisation of exogenous NR and, more surprisingly, NMN. Without expression of the NRK enzymes in tissues, the NAD+-boosting effects of nicotinamide riboside (NR) and NMN supplementation is blocked, whilst expression of alternative NAD+ biosynthesis enzymes remains comparable to wild-type mice. Phosphorylation of NR by NRK1 appears preferred to NRK2 even in skeletal muscle where Nmrk2 is specifically expressed and found at substantially higher mRNA levels than Nmrk1. In NAD+ deficiency, NRK2 may be induced to aid NAD+ biosynthesis. NRK2 appears to play a redundant role in NAD+ biosynthesis along with NRK1, at least in unchallenged models, its highly regulated expression particularly in times of stress suggest it may have role beyond NAD+ metabolism
physiological function
nicotinamide riboside kinase-2 (NRK-2) is a muscle-specific beta1 integrin binding protein, that is predominantly expressed in skeletal muscle with a trace amount expressed in healthy cardiac tissue. Nicotinamide riboside kinase-2 alleviates ischemia-induced heart failure through P38 signaling, role of NRK-2 in ischemia-induced cardiac remodeling and dysfunction, overview. NRK-2 plays a role in the NAD+ salvage pathway, but the role of NRK-2 in NAD+ synthesis is dispensable. NRK-2 may regulate cardiac pathophysiology of heart failure. NRK-2 mitigates TGF-beta-induced myofibroblast transformation
physiological function
NRK2 appears to play a redundant role in NAD+ biosynthesis along with NRK1, at least in unchallenged models, its highly regulated expression particularly in times of stress suggest it may have role beyond NAD+ metabolism
physiological function
NRK2 appears to play a redundant role in NAD+ biosynthesis along with NRK1, at least in unchallenged models, its highly regulated expression particularly in times of stress suggest it may have role beyond NAD+ metabolism
physiological function
NRK2 is dispensable in H6PD-KO myopathy
physiological function
-
upregulation of nicotinamide riboside kinase 2 (NRK2) mediated salvage of nicotinamide riboside into NAD+ is an early adaptation to perturbed muscle sarcoplasmic reticulum NAD(P)(H) homeostasis and impaired mitochondrial energy production in hexose-6-posphate dehydrogenase deficiency
-
physiological function
-
NRK2 is dispensable in H6PD-KO myopathy
-
physiological function
-
nicotinamide riboside kinase-2 (NRK-2) is a muscle-specific beta1 integrin binding protein, that is predominantly expressed in skeletal muscle with a trace amount expressed in healthy cardiac tissue. Nicotinamide riboside kinase-2 alleviates ischemia-induced heart failure through P38 signaling, role of NRK-2 in ischemia-induced cardiac remodeling and dysfunction, overview. NRK-2 plays a role in the NAD+ salvage pathway, but the role of NRK-2 in NAD+ synthesis is dispensable. NRK-2 may regulate cardiac pathophysiology of heart failure. NRK-2 mitigates TGF-beta-induced myofibroblast transformation
-
additional information
proposed NRK expression in disease and potential therapeutic interventions
additional information
proposed NRK expression in disease and potential therapeutic interventions
additional information
proposed NRK expression in disease and potential therapeutic interventions
additional information
proposed NRK expression in disease and potential therapeutic interventions
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Rowen, J.W.; Kornberg, A.
The phosphorolysis of nicotinamide riboside
J. Biol. Chem.
193
497-507
1951
Sus scrofa
brenda
Singh, S.K.; Kurnasov, O.V.; Chen, B.; Robinson, H.; Grishin, N.V.; Osterman, A.L.; Zhang, H.
Crystal structure of Haemophilus influenzae NadR protein. A bifunctional enzyme endowed with NMN adenyltransferase and ribosylnicotinimide kinase activities
J. Biol. Chem.
277
33291-33299
2002
Haemophilus influenzae
brenda
Kurnasov, O.V.; Polanuyer, B.M.; Ananta, S.; Sloutsky, R.; Tam, A.; Gerdes, S.Y.; Osterman, A.L.
Ribosylnicotinamide kinase domain of NadR protein: identification and implications in NAD biosynthesis
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Escherichia coli, Salmonella enterica, Haemophilus influenzae (Q57425), Haemophilus influenzae
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Regulation of NAD synthesis by the trifunctional NadR protein of Salmonella enterica
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Salmonella enterica
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Belenky, P.; Racette, F.G.; Bogan, K.L.; McClure, J.M.; Smith, J.S.; Brenner, C.
Nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+
Cell
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473-484
2007
Saccharomyces cerevisiae (P53915)
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Merdanovic, M.; Sauer, E.; Reidl, J.
Coupling of NAD+ biosynthesis and nicotinamide ribosyl transport: characterization of NadR ribonucleotide kinase mutants of Haemophilus influenzae
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Khan, J.A.; Xiang, S.; Tong, L.
Crystal structure of human nicotinamide riboside kinase
Structure
15
1005-1013
2007
Homo sapiens (Q9NWW9), Homo sapiens
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Zamporlini, F.; Ruggieri, S.; Mazzola, F.; Amici, A.; Orsomando, G.; Raffaelli, N.
Novel assay for simultaneous measurement of pyridine mononucleotides synthesizing activities allows dissection of the NAD+ biosynthetic machinery in mammalian cells
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Homo sapiens
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Nicotinamide riboside kinase-2 alleviates ischemia-induced heart failure through P38 signaling
Biochim. Biophys. Acta
1866
165609
2020
Mus musculus (Q9D7C9), Mus musculus, Homo sapiens (Q9NPI5), Homo sapiens, Mus musculus C57BL/6N (Q9D7C9)
brenda
Fletcher, R.S.; Ratajczak, J.; Doig, C.L.; Oakey, L.A.; Callingham, R.; Da Silva Xavier, G.; Garten, A.; Elhassan, Y.S.; Redpath, P.; Migaud, M.E.; Philp, A.; Brenner, C.; Canto, C.; Lavery, G.G.
Nicotinamide riboside kinases display redundancy in mediating nicotinamide mononucleotide and nicotinamide riboside metabolism in skeletal muscle cells
Mol. Metab.
6
819-832
2017
Mus musculus (Q91W63), Mus musculus (Q9D7C9)
brenda
Sambeat, A.; Ratajczak, J.; Joffraud, M.; Sanchez-Garcia, J.L.; Giner, M.P.; Valsesia, A.; Giroud-Gerbetant, J.; Valera-Alberni, M.; Cercillieux, A.; Boutant, M.; Kulkarni, S.S.; Moco, S.; Canto, C.
Endogenous nicotinamide riboside metabolism protects against diet-induced liver damage
Nat. Commun.
10
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Mus musculus (Q91W63)
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Ratajczak, J.; Joffraud, M.; Trammell, S.A.; Ras, R.; Canela, N.; Boutant, M.; Kulkarni, S.S.; Rodrigues, M.; Redpath, P.; Migaud, M.E.; Auwerx, J.; Yanes, O.; Brenner, C.; Canto, C.
NRK1 controls nicotinamide mononucleotide and nicotinamide riboside metabolism in mammalian cells
Nat. Commun.
7
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Mus musculus
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Doig, C.L.; Zielinska, A.E.; Fletcher, R.S.; Oakey, L.A.; Elhassan, Y.S.; Garten, A.; Cartwright, D.; Heising, S.; Alsheri, A.; Watson, D.G.; Prehn, C.; Adamski, J.; Tennant, D.A.; Lavery, G.G.
Induction of the nicotinamide riboside kinase NAD+ salvage pathway in a model of sarcoplasmic reticulum dysfunction
Skeletal Muscle
10
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2020
Mus musculus (Q9D7C9), Mus musculus C57/BL6J (Q9D7C9)
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Fletcher, R.S.; Lavery, G.G.
The emergence of the nicotinamide riboside kinases in the regulation of NAD+ metabolism
J. Mol. Endocrinol.
61
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Danio rerio (F1QSN9), Homo sapiens (Q9NPI5), Homo sapiens (Q9NWW6), Mus musculus (Q91W63), Mus musculus (Q9D7C9)
brenda