EC Number   |
Application |
Reference |
|---|
    2.3.1.21 | medicine |
compared to isoforms CPT1A, CPT1B and CPT2, isoform CPT1C exerts the most significant effect on mitochondrial dysfunction-associated tumor cellular senescence among the members of the CPT family |
757297 |
| 2.3.1.21 | medicine |
enzyme inhibitors are used to shift the heart's reliance away from fatty acid oxidation to glucose as energy source to increase cardiac efficiency, overview |
673216 |
| 2.3.1.21 | medicine |
hypertrophied myocardium displays a significant shift in the relative isoform distribution of CPT1 isoforms, L-CPT1 expression dramatically increases relative to M-CPT1 expression |
686125 |
| 2.3.1.21 | medicine |
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 | medicine |
overexpression of the enzyme correlates with a poor overall survival of ovarian cancer patients. CPT1A is a prognostic biomarker and rational target for therapeutic intervention of cancer |
736916 |
| 2.3.1.21 | medicine |
problems in CPT2 deficiency originating from the S113L mutation might be at least partially related to an impaired thermal stability of the protein |
757810 |
| 2.3.1.21 | medicine |
the data suggest that consuming a high-fat diet or inhibiting CPT-I do not result in cardiac hypertrophy or cardiac dysfunction in normal rats |
686180 |
| 2.3.1.21 | medicine |
treatment of CPT2 deficiency is based upon avoidance of fasting and/or exercise, a low fat diet enriched with medium chain triglycerides and carnitine |
659899 |
| 2.3.1.21 | medicine |
triple-negative breast cancer cells resistant to glutaminase inhibitor CB-839 have increased CPT2 protein and CPT1 activity levels. CB-839-resistant triple-negative breast cancer cells mobilize more fatty acids into mitochondria for oxidation |
757235 |
| 2.3.1.21 | medicine |
triple-negative breast cancer cells resistant to glutaminase inhibitor CB-839 have increased CPT2 protein and CPT1 activity levels. CB-839-resistant triple-negative breast cancer cells mobilize more fatty acids into mitochondria for oxidation. Inhibition of both glutaminase and CPT1 decreases cell proliferation and migration of CB-839-resistant cells compared with single inhibition of each enzyme |
757235 |
