EC Number   |
General Information |
Reference |
|---|
    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) |
761705 |
| 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) |
761705 |
| 2.7.1.22 | 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 |
-, 760203 |
| 2.7.1.22 | 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 |
-, 758846 |
| 2.7.1.22 | malfunction |
loss of NRK-2 enhances p38alpha activation following ischemic injury |
-, 758846 |
| 2.7.1.22 | malfunction |
nicotinamide riboside kinase 2 (NRK2) deficiency alone has minimal impact in wild-type mice |
-, 760203 |
| 2.7.1.22 | 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 |
758846 |
| 2.7.1.22 | 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 |
759821 |
| 2.7.1.22 | malfunction |
NRK1, NRK2, and double KO myotubes reveal redundancy in the nicotinamide riboside kinase dependent metabolism of nicotinamide riboside to NAD+ |
759784 |
| 2.7.1.22 | 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+ |
759784 |
