EC Number   |
General Information |
Reference |
|---|
    6.2.1.1 | physiological function |
acetyl-CoA synthetase 2 is a regulator of autophagy and lifespan |
744651 |
| 6.2.1.1 | physiological function |
acetyl-coenzyme A synthetase activates acetate into acetyl-coenzyme A in most cells. Salmonella enterica requires Acs activity for growth on acetate. The sirtuin-dependent protein acylation/deacylation system, SDPADS, controls the activity of Acs |
716267 |
| 6.2.1.1 | physiological function |
activation of acetate in energy metabolism |
-, 726837 |
| 6.2.1.1 | physiological function |
an acs2 deletion strain has a reduced replicative life span compared to wild-type and isoform acs1 deletion strains. Replicatively aged acs2 deletion cells contain elevated levels of extrachromosomal rDNA circles, and silencing at the rDNA locus is impaired in an acs2 deletion strain |
705678 |
| 6.2.1.1 | physiological function |
enzyme overexpression results in higher resistance to acetic acid as measured by an increased growth rate and shorter lag phase relative to a wild type strain, suggesting that enzyme-mediated consumption of acetic acid during fermentation contributes to acetic acid detoxification |
744932 |
| 6.2.1.1 | physiological function |
enzyme-mediated acetyl-CoA synthesis from acetate is necessary for human cytomegalovirus infection and can compensate for the loss of ATP-citrate lyase |
746321 |
| 6.2.1.1 | physiological function |
isoform ACSS2 is an important factor for promoting renal cell carcinoma development and is essential for cell migration and invasion |
744665 |
| 6.2.1.1 | physiological function |
the enzyme regulates histone acetylation and hippocampal memory |
745887 |
| 6.2.1.1 | physiological function |
the high-affinity biosynthetic pathway for converting acetate to acetyl-coenzyme A (acetyl-CoA) is catalyzed by the central metabolic enzyme acetyl-coenzyme A synthetase (Acs), which is finely regulated both at the transcriptional level via cyclic AMP (cAMP)-driven trans-activation and at the post-translational level via acetylation inhibition. The cAMP contact residues are well conserved from prokaryotes to eukaryotes, suggesting a general regulatory mechanism of cAMP on Acs. cAMP generally inhibits other acyl- or aryl-CoA synthetases |
-, 745369 |
| 6.2.1.1 | physiological function |
tumor cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells |
703038 |
