EC Number |
General Information |
Reference |
---|
2.4.2.12 | malfunction |
enzyme inhibition induces NAD depletion in various mouse organs but selectively causes dramatic atrophy of the spleen red pulp |
736227 |
2.4.2.12 | malfunction |
enzyme inhibition is responsible for ATP depletion, metabolic perturbation, and subsequent tumor growth inhibition |
736436 |
2.4.2.12 | malfunction |
homozygous enzyme knockout results in lethality at an early stage of mouse embryonic development and death within 5-10 days in adult mice accompanied by a 25.24% body weight loss |
759022 |
2.4.2.12 | malfunction |
implicated in the pathogenesis of a number of human diseases or conditions such as acute lung injury, aging, atherosclerosis, cancer, diabetes, rheumatoid arthritis and sepsis |
722560 |
2.4.2.12 | malfunction |
partial deletion of the enzyme facilitates high-fat diet-induced atrial fibrillation through increased diastolic calcium leaks |
759372 |
2.4.2.12 | malfunction |
reduced enzyme expression increases endothelial cell susceptibility to tumor necrosis factor-alpha-induced apoptosis as reflected by PARP-1 cleavage and caspase-3 activation |
758625 |
2.4.2.12 | metabolism |
enhanced enzyme expression increases cellular NAD+ concentration no more than 2fold |
760043 |
2.4.2.12 | metabolism |
enzyme-mediated NAD biosynthesis may modify cocaine behavioral effects through sirtuin 1. The enzyme regulates cocaine reward through the NAD/sirtuin 1 pathway |
759157 |
2.4.2.12 | metabolism |
the enzyme catalyzes the rate-limiting step in NAD synthesis |
759503 |
2.4.2.12 | physiological function |
cardiac-specific overexpression of Nampt in transgenic mice increases NAD+ content in the heart, prevents downregulation of Nampt, and reduces the size of myocardial infarction and apoptosis in response to prolonged ischemia and ischemia/reperfusion. Upregulation of Nampt significantly increases NAD+ and ATP concentrations, whereas downregulation of Nampt significantly decreases them. Expression of Nampt in the heart is significantly decreased by ischemia, ischemia/reperfusion and pressure overload. Downregulation of Nampt increases caspase 3 cleavage, cytochrome c release, and TUNEL-positive cells, which are inhibited in the presence of Bcl-xL, but do not increase hairpin 2-positive cells, suggesting that endogenous Nampt negatively regulates apoptosis but not necrosis. Downregulation of Nampt also impairs autophagic flux |
703243 |