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Literature summary extracted from

  • Fletcher, R.S.; Lavery, G.G.
    The emergence of the nicotinamide riboside kinases in the regulation of NAD+ metabolism (2018), J. Mol. Endocrinol., 61, R107-R121 .
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

EC Number Cloned (Comment) Organism
2.7.1.22 gene NMRK1 Homo sapiens
2.7.1.22 gene NMRK1 Mus musculus
2.7.1.22 gene NMRK2 Homo sapiens
2.7.1.22 gene NMRK2 Mus musculus
2.7.1.22 gene NMRK2 Danio rerio
2.7.1.173 gene NMRK1 Homo sapiens
2.7.1.173 gene NMRK2 Homo sapiens

KM Value [mM]

EC Number KM Value [mM] KM Value Maximum [mM] Substrate Comment Organism Structure
2.7.1.22 0.068
-
 1-(beta-D-ribofuranosyl)-nicotinamide pH and temperature not specified in the publication, with GTP Homo sapiens
2.7.1.22 0.088
-
 1-(beta-D-ribofuranosyl)-nicotinamide pH and temperature not specified in the publication, with ATP Homo sapiens
2.7.1.22 0.19
-
 1-(beta-D-ribofuranosyl)-nicotinamide with ATP, pH and temperature not specified in the publication Homo sapiens
2.7.1.22 30
-
 1-(beta-D-ribofuranosyl)-nicotinamide with GTP, pH and temperature not specified in the publication Homo sapiens
2.7.1.173 0.051
-
 beta-D-ribosylnicotinate with ATP, pH and temperature not specified in the publication Homo sapiens
2.7.1.173 0.063
-
 beta-D-ribosylnicotinate with ATP, pH and temperature not specified in the publication Homo sapiens

Metals/Ions

EC Number Metals/Ions Comment Organism Structure
2.7.1.22 Mg2+ required Homo sapiens
2.7.1.22 Mg2+ required Mus musculus
2.7.1.22 Mg2+ required Danio rerio
2.7.1.173 Mg2+ required Homo sapiens

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
2.7.1.22 ATP + 1-(beta-D-ribofuranosyl)-nicotinamide Homo sapiens
-
 ADP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 ATP + 1-(beta-D-ribofuranosyl)-nicotinamide Mus musculus
-
 ADP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 ATP + 1-(beta-D-ribofuranosyl)-nicotinamide Danio rerio
-
 ADP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 GTP + 1-(beta-D-ribofuranosyl)-nicotinamide Homo sapiens
-
 GDP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 GTP + 1-(beta-D-ribofuranosyl)-nicotinamide Mus musculus
-
 GDP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.173 ATP + beta-D-ribosylnicotinate Homo sapiens
-
 ADP + nicotinate beta-D-ribonucleotide
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
2.7.1.22 Danio rerio F1QSN9
-
-
2.7.1.22 Homo sapiens Q9NPI5
-
-
2.7.1.22 Homo sapiens Q9NWW6
-
-
2.7.1.22 Mus musculus Q91W63
-
-
2.7.1.22 Mus musculus Q9D7C9
-
-
2.7.1.173 Homo sapiens Q9NPI5
-
-
2.7.1.173 Homo sapiens Q9NWW6
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
2.7.1.22 brown adipose tissue
-
 Mus musculus
-
2.7.1.22 kidney
-
 Mus musculus
-
2.7.1.22 liver
-
 Mus musculus
-
2.7.1.22 skeletal muscle
-
 Mus musculus
-
2.7.1.22 skeletal muscle high expression of NRK2 Mus musculus
-
2.7.1.22 spinal ganglion
-
 Mus musculus
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2.7.1.22 ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
-
 Homo sapiens ADP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
-
 Mus musculus ADP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 ATP + 1-(beta-D-ribofuranosyl)-nicotinamide
-
 Danio rerio ADP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
-
 Homo sapiens GDP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 GTP + 1-(beta-D-ribofuranosyl)-nicotinamide
-
 Mus musculus GDP + beta-nicotinamide D-ribonucleotide
-
 ?
2.7.1.22 additional information enzyme NRK2 highly prefers ATP, while isozyme NRK1 also uses GTP with similar activity Homo sapiens ?
-
-
2.7.1.22 additional information enzyme NRK2 is restricted to ATP, while isozyme NRK1 also uses GTP Mus musculus ?
-
-
2.7.1.173 ATP + beta-D-ribosylnicotinate
-
 Homo sapiens ADP + nicotinate beta-D-ribonucleotide
-
 ?

Synonyms

EC Number Synonyms Comment Organism
2.7.1.22 More see also EC 2.7.1.173 Homo sapiens
2.7.1.22 nicotinamide riboside kinase 1
-
 Homo sapiens
2.7.1.22 nicotinamide riboside kinase 1
-
 Mus musculus
2.7.1.22 nicotinamide riboside kinase 2
-
 Homo sapiens
2.7.1.22 nicotinamide riboside kinase 2
-
 Mus musculus
2.7.1.22 nicotinamide riboside kinase 2
-
 Danio rerio
2.7.1.22 NMRK1
-
 Homo sapiens
2.7.1.22 NMRK2
-
 Homo sapiens
2.7.1.22 NMRK2
-
 Danio rerio
2.7.1.22 NRK1
-
 Homo sapiens
2.7.1.22 NRK1
-
 Mus musculus
2.7.1.22 Nrk2
-
 Homo sapiens
2.7.1.22 Nrk2
-
 Mus musculus
2.7.1.22 Nrk2b
-
 Danio rerio
2.7.1.173 More see also EC 2.7.1.22 Homo sapiens
2.7.1.173 nicotinamide riboside kinase 1
-
 Homo sapiens
2.7.1.173 nicotinamide riboside kinase 2
-
 Homo sapiens
2.7.1.173 NMRK1
-
 Homo sapiens
2.7.1.173 NMRK2
-
 Homo sapiens
2.7.1.173 NRK1
-
 Homo sapiens
2.7.1.173 Nrk2
-
 Homo sapiens

Turnover Number [1/s]

EC Number Turnover Number Minimum [1/s] Turnover Number Maximum [1/s] Substrate Comment Organism Structure
2.7.1.22 0.34
-
 1-(beta-D-ribofuranosyl)-nicotinamide pH and temperature not specified in the publication, with GTP Homo sapiens
2.7.1.22 0.6
-
 1-(beta-D-ribofuranosyl)-nicotinamide pH and temperature not specified in the publication, with ATP Homo sapiens
2.7.1.22 0.75
-
 1-(beta-D-ribofuranosyl)-nicotinamide with ATP, pH and temperature not specified in the publication Homo sapiens
2.7.1.22 1.7
-
 1-(beta-D-ribofuranosyl)-nicotinamide with GTP, pH and temperature not specified in the publication Homo sapiens
2.7.1.173 0.21
-
 beta-D-ribosylnicotinate with ATP, pH and temperature not specified in the publication Homo sapiens
2.7.1.173 0.34
-
 beta-D-ribosylnicotinate with ATP, pH and temperature not specified in the publication Homo sapiens

Cofactor

EC Number Cofactor Comment Organism Structure
2.7.1.22 ATP
-
 Homo sapiens
2.7.1.22 ATP
-
 Mus musculus
2.7.1.22 ATP
-
 Danio rerio
2.7.1.22 GTP
-
 Homo sapiens
2.7.1.22 GTP
-
 Mus musculus
2.7.1.173 ATP
-
 Homo sapiens

Expression

EC Number Organism Comment Expression
2.7.1.22 Mus musculus following injury to dorsal root ganglion neurons, Nmrk2 is the most upregulated NAD+ biosynthetic gene (by over 20fold). Mice with a loss of hexose-6-phosphate dehydrogenase (H6PDH) function, an ER-based enzyme required for local NADPH generation, manifest with severe muscle myopathy and on transcriptional analysis Nmrk2 expression is the most dysregulated gene (upregulated by over 60fold mRNA level). Nmrk2 mRNA expression is substantially induced (over 80fold) in models of lethal cardiomyopathy up
2.7.1.22 Homo sapiens Nmrk2 mRNA expression is substantially induced (over 80fold) in models of lethal cardiomyopathy up
2.7.1.173 Homo sapiens Nmrk2 mRNA expression is substantially induced (over 80fold) in models of lethal cardiomyopathy up

General Information

EC Number General Information Comment Organism
2.7.1.22 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) Mus musculus
2.7.1.22 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) Mus musculus
2.7.1.22 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 Danio rerio
2.7.1.22 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 Homo sapiens
2.7.1.22 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 Mus musculus
2.7.1.22 additional information proposed NRK expression in disease and potential therapeutic interventions Homo sapiens
2.7.1.22 additional information proposed NRK expression in disease and potential therapeutic interventions Mus musculus
2.7.1.22 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 Mus musculus
2.7.1.22 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 Mus musculus
2.7.1.22 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 Homo sapiens
2.7.1.22 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 Danio rerio
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), see for EC 2.7.1.22. 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) Homo sapiens
2.7.1.173 additional information proposed NRK expression in disease and potential therapeutic interventions Homo sapiens
2.7.1.173 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 Homo sapiens

kcat/KM [mM/s]

EC Number kcat/KM Value [1/mMs-1] kcat/KM Value Maximum [1/mMs-1] Substrate Comment Organism Structure
2.7.1.22 0.057
-
 1-(beta-D-ribofuranosyl)-nicotinamide with GTP, pH and temperature not specified in the publication Homo sapiens
2.7.1.22 3.95
-
 1-(beta-D-ribofuranosyl)-nicotinamide with ATP, pH and temperature not specified in the publication Homo sapiens
2.7.1.22 5
-
 1-(beta-D-ribofuranosyl)-nicotinamide pH and temperature not specified in the publication, with GTP Homo sapiens
2.7.1.22 6.82
-
 1-(beta-D-ribofuranosyl)-nicotinamide pH and temperature not specified in the publication, with ATP Homo sapiens
2.7.1.173 4.12
-
 beta-D-ribosylnicotinate with ATP, pH and temperature not specified in the publication Homo sapiens
2.7.1.173 5.4
-
 beta-D-ribosylnicotinate with ATP, pH and temperature not specified in the publication Homo sapiens