EC Number   |
General Information |
Reference |
|---|
    2.3.3.8 | metabolism |
modulation of ACLY expression correlates with the development and progressions of various chronic diseases such as neurodegenerative diseases, cardiovascular diseases, diabetes, obesity, inflammation, and cancer. Inhibition of ACLY activity modulates the glycolysis and lipogenesis processes and stimulates normal physiological functions |
757453 |
| 2.3.3.8 | metabolism |
regulatory role of ACLY activity in chondrocyte matrix homeostasis by modulation of the nucleocytosolic pool of acetyl-CoA, which impacted on catabolic and anabolic responses via post-translational and epigenetic modifications. Increased ACLY activity in osteoarthritis chondrocytes increases nucleocytosolic acetyl-CoA, leading to increased matrix catabolism via dysregulated histone and transcription factor acetylation |
757200 |
| 2.3.3.8 | metabolism |
the enzyme catalyzes the formation of cytosolic acetyl CoA, the starting material for de novo lipid and cholesterol biosynthesis |
756189 |
| 2.3.3.8 | metabolism |
the enzyme controls a glucose-to-acetate metabolic switch |
756391 |
| 2.3.3.8 | metabolism |
the enzyme is a major source of nucleocytosolic acetyl-CoA, a fundamental building block of carbon metabolism in eukaryotes |
757232 |
| 2.3.3.8 | metabolism |
the enzyme is an epigenetic regulator that promotes renal ectopic lipid accumulation and fibrogenesis leading to renal injury in obesity. Induction of ATP-citrate lyase in in the kidney of overweight or obese patients with chronic kidney disease is associated with increased ectopic lipid accumulation, glomerulosclerosis, and albuminuria. Acetyl-CoA is the substrate for de novo lipogenesis as well as for histone acetylation. By raising acetyl-CoA concentration ATP-citrate lyase promotes H3K9/14 and H3K27 hyperacetylation leading to up-regulation of several rate-limiting lipogenic enzymes and fibrogenic factors. On the other hand, the excess acetyl-CoA generated as a result of ATP-citrate lyase induction provides the substrate for these lipogenic enzymes to drive de novo lipogenesis leading to ectopic lipid accumulation, a detrimental event toward renal injury |
756693 |
| 2.3.3.8 | metabolism |
the enzyme is involved in citrate metabolism |
718760 |
| 2.3.3.8 | metabolism |
the enzyme links carbohydrate and lipid metabolism |
757804 |
| 2.3.3.8 | metabolism |
the enzyme links energy metabolism provided by catabolic pathways to biosynthesis. ACLY plays a pivotal role in cancer metabolism through the potential deprivation of cytosolic citrate, a process promoting glycolysis through the enhancement of the activities of PFK 1 and 2 with concomitant activation of oncogenic drivers such as PI3K/AKT which activate ACLY and the Warburg effect in a feed-back loop |
756333 |
| 2.3.3.8 | metabolism |
the enzyme plays a critical role in epigenetic regulation of diabetic renal fibrosis. It is essential for high glucose-induced histone hyperacetylation and fibrogenic gene upregulation in mesangial cells |
755769 |
