EC Number   |
Application |
Reference |
|---|
    2.3.3.8 | analysis |
coupled fluorometric assay for EC 2.3.1.1 based on coupling coenzyme A production to the oxidation of NADH via ATP-citrate lyase and malate dehydrogenase |
488185 |
| 2.3.3.8 | drug development |
Mendelian randomization of large human cohorts has validated ACLY as a promising target for low-density-lipoprotein-cholesterol lowering and cardiovascular protection |
758267 |
| 2.3.3.8 | drug development |
the dysfunction and upregulation of ATP citrate lyase in numerous cancers makes it an attractive target for developing anticancer therapies. ATP citrate lyase inhibition by shRNA knockdown limits cancer cell proliferation and reduces cancer stemness |
756189 |
| 2.3.3.8 | drug development |
the enzyme is a target for anticancer drugs, because many cancer cells depend on its activity for proliferation. ACLY is also a target against dyslipidaemia and hepatic steatosis. Under physiological conditions, citrate carries three negative charges and establishes predominantly hydrophilic and ionic interactions with the enzyme in its binding site, which would not be optimal for drug discovery. The extensive conformational changes observed here reveal a hydrophobic cavity in the core of the citrate domain allowing the high-affinity binding of more hydrophobic and drug-like molecules such as NDI-091143. The allosteric site offers an attractive target for the development of ACLY inhibitors |
757803 |
| 2.3.3.8 | medicine |
3,5-dichloro-2-hydroxy-N-(4-methoxybiphenyl-3-yl)benzenesulfonamide is a cell-permeable inhibitor with modest potency. It shows an oral availability of 55%, but a half-life of only 2.1 h. After 20 days of treatment, there is a modest lowering of both plasma cholesterol and triglycerides in high-fat fed mice |
672624 |
| 2.3.3.8 | medicine |
ATP citrate synthase inhibition by RNAi or the chemical SB-204990 limits in vitro proliferation and survival of tumor cells displaying aerobic glycolysis |
672878 |
| 2.3.3.8 | medicine |
ATP citrate synthase inhibition by RNAi or the chemical SB-204990 limits in vitro proliferation and survival of tumor cells displaying aerobic glycolysis. The same treatments also reduce in vivo tumor growth and induce differentiation |
672878 |
| 2.3.3.8 | medicine |
diabetic patients in resting conditions and after activation with thrombin, show higher enzyme activity than controls, accompanied by increased pyruvate dehydrogenase activity, acetyl-CoA content, and thrombin-evoked malonyl dialdehyde synthesis. Activation of diabetic platelets causes 2 times greater release of acetyl-CoA from their mitochondria than in controls |
659852 |
| 2.3.3.8 | medicine |
renal stone patients have low urinary citrate excretion with high leukocyte ATP citrate (pro-3S)-lyase activity. In Northeast Thailand, low potassium status and a high carbohydrate and low fat diet may cause the increased enzyme activity. Hypokaliuria and high leukocyte ATP citrate (pro-3S)-lyase activity can be corrected by potassium-sodium citrate salt therapy |
488219 |
| 2.3.3.8 | medicine |
stable knockdown of ATP citrate synthase significantly impairs Akt-mediated tumorigenesis in vivo |
676255 |
