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Literature summary for 2.3.3.8 extracted from
- ATP-citrate lyase is an epigenetic regulator to promote obesity-related kidney injury (2019), FASEB J., 33, 9602-9615 .
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + citrate + CoA | Homo sapiens | - |
ADP + phosphate + acetyl-CoA + oxaloacetate | - |
? |  |
| ATP + citrate + CoA | Mus musculus | - |
ADP + phosphate + acetyl-CoA + oxaloacetate | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | P53396 | - |
- |
| Mus musculus | Q91V92 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| kidney | cortex | Mus musculus | - |
| mesangial cell | - |
Homo sapiens | - |
| mesangial cell | - |
Mus musculus | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + citrate + CoA | - |
Homo sapiens | ADP + phosphate + acetyl-CoA + oxaloacetate | - |
? | |
| ATP + citrate + CoA | - |
Mus musculus | ADP + phosphate + acetyl-CoA + oxaloacetate | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| ACL | - |
Homo sapiens |
| ACL | - |
Mus musculus |
| ATP-citrate lyase | - |
Homo sapiens |
| ATP-citrate lyase | - |
Mus musculus |
Expression
| Organism | Comment | Expression |
|---|---|---|
| Mus musculus | highly induced in ob/ob BTBR mice | up |
| Homo sapiens | highly induced in the kidney of overweight or obese patients with chronic kidney disease. Induction 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 | up |
| Homo sapiens | in mesangial cells, the enzyme is synergistically induced by high glucose, palmitate, and TNF-alpha via NF-kapaB and PKA pathways | up |
General Information
| General Information | Comment | Organism |
|---|---|---|
| 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 | Homo sapiens |
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