EC Number   |
General Information |
Reference |
|---|
    2.3.1.21 | malfunction |
enzyme deficiency leads to a significant decrease in fatty acid beta-oxidation and adenosine triphosphate generation, combined with a reduced mitochondrial membrane potential, resulting in cellular apoptosis |
737070 |
| 2.3.1.21 | malfunction |
enzyme inactivation inhibits cell growth and ATP production and decreases tumorigenicity of ovarian cancer cells in severe combined immunodeficiency mice |
736916 |
| 2.3.1.21 | metabolism |
arnitine palmitoyltransferase-1 is the critical enzyme for mitochondrial beta-oxidation of long-chain fatty acids |
736183 |
| 2.3.1.21 | metabolism |
the enzyme is crucial for mitochondrial acylcarnitine formation and export to the extracellular fluids in mitochondrial fatty acid beta-oxidation disorders |
736077 |
| 2.3.1.21 | physiological function |
CPT1C expression correlates inversely with mammalian target of rapamycin pathway activation, and contributes to rapamycin resistance in murine primary tumors. Tumor cells constitutively expressing CPT1C show increased fatty acid oxidation, ATP production, and resistance to glucose deprivation or hypoxia. Cancer cells lacking CPT1C produce less ATP and are more sensitive to metabolic stress. CPT1C depletion via siRNA suppresses xenograft tumor growth and metformin responsiveness in vivo |
719554 |
| 2.3.1.21 | physiological function |
fasting does not significantly change Vmax and free carnitine content in liver. Catalytic efficiency (Vmax/Km) and the ratio free carnitine/Km increases in fish fasted for 4 days. Both indicators decline when fish fast for 12 days |
756509 |
| 2.3.1.21 | physiological function |
heterologous expression of a constitutively active CPT1A variant in brown adipocyte cells leads to increased fatty acid oxidation, lipolysis, UCP1 protein levels and mitochondrial activity. Enhanced fatty acid oxidation reduces the palmitate-induced increase in triglyceride content and the expression of obese and inflammatory markers |
758136 |
| 2.3.1.21 | physiological function |
isoform CPT1C expression is frequently up-regulated in human lung tumors. Tumor cells constitutively expressing CPT1C show increased fatty acid oxidation, ATP production, and resistance to glucose deprivation or hypoxia. Conversely, cancer cells lacking CPT1C produce less ATP and are more sensitive to metabolic stress. CPT1Cdepletion via siRNA suppresses xenograft tumor growth and metformin responsiveness in vivo. CPT1C can be induced by hypoxia or glucose deprivation and is regulated by AMPKalpha |
719554 |
| 2.3.1.21 | physiological function |
measurements of enzyme activity in mitochondria isolated from newborn, 24-h-old, fed or fasted, and 5-months-old pigs. Acetate rather than ketone bodies is the predominant radiolabeled product, and its production increases twofold with increasing fatty acid oxidation during the first 24-h suckling period. The rate of acetogenesis is directly proportional to isoform CPT I activity. The high activity of CPT I in 24-h-suckling piglets is not attributable to an increase in CPT I gene expression, but rather to a large decrease in the sensitivity of CPT I to malonyl-CoA inhibition, which offsets a developmental decrease in affinity of CPT I for palmitoyl-CoA. Acetate is the primary product of hepatic mitochondrial beta-oxidation in Sus scrofa and regulation during early development is mediated primarily via kinetic modulation of isoform CPT I. |
718550 |
| 2.3.1.21 | physiological function |
ovarian cancer cells depend on or are addicted to enzyme-mediated fatty acid beta-oxidation for cell cycle progression |
736916 |
