2.7.1.22: ribosylnicotinamide kinase
This is an abbreviated version!
For detailed information about ribosylnicotinamide kinase, go to the full flat file.
Reaction
Synonyms
kinase, ribosylnicotinamide (phosphorylating), More, muscle-specific beta1 integrin binding protein, NadR, nicotinamide ribose kinase, nicotinamide riboside kinase, nicotinamide riboside kinase 1, nicotinamide riboside kinase 2, nicotinamide riboside kinase-2, NmR-K, NMRK1, NMRK2, NR kinase 1, Nrk, NRK-2, NRK1, Nrk2, Nrk2b
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General Information
General Information on EC 2.7.1.22 - ribosylnicotinamide kinase
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malfunction
metabolism
physiological function
additional information
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
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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
-
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
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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
-
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
-
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
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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