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2.3.3.8: ATP citrate synthase

This is an abbreviated version!
For detailed information about ATP citrate synthase, go to the full flat file.

Word Map on EC 2.3.3.8

Reaction

ADP
+
phosphate
 +
acetyl-CoA
 +
oxaloacetate
=
ATP
 +
citrate
 +
CoA

Synonyms

ACL, ACL1, ACL2, ACLA, ACLB, ACLY, adenosine triphosphate citrate lyase, ATP citrate (pro-S)-lyase, ATP citrate lyase, ATP citrate lyase isoform 2, ATP-citrate lyase, ATP-citrate synthase A-2, ATP-citrate synthase alpha chain protein 2, ATP-citric lyase, ATP:citrate lyase, ATP:citrate oxaloacetate lyase ((pro-3S)-CH2COO--> acetyl-CoA) (ATP-dephosphorylating), ATP:citrate oxaloacetate-lyase (pro-3S-CH2COO->acetyl-CoA, ATP dephosphorylating), ATP:citrate oxaloacetate-lyase CoA-acetylating and ATP-dephosphorylating, Citrate cleavage enzyme, citrate-ATP lyase, citric cleavage enzyme, Earlier Degraded Tapetum1, EC 4.1.3.8, EDT1, Os11g0696200

ECTree

     2 Transferases
         2.3 Acyltransferases
             2.3.3 Acyl groups converted into alkyl groups on transfer
                2.3.3.8 ATP citrate synthase

Expression

Expression on EC 2.3.3.8 - ATP citrate synthase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
48 h after exhaustion of nitrogen in the culture, the enzyme shows marked decrease (84%) in activity. The enzyme activity decreases in a time period of 20-100 h during lipid accumulation
enzyme activity increases with dissolved oxygen and upon ammonium depletion in an ammonium-limited culture
enzyme mRNA and protein levels markedly (about 2.5fold) and quickly increase in activated macrophages. Tumour necrosis factor alpha and interferon gamma upregulate enzyme gene expression
-
high glucose upregulates ATP-citrate lyase expression
highly induced in ob/ob BTBR mice
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
in mesangial cells, the enzyme is synergistically induced by high glucose, palmitate, and TNF-alpha via NF-kapaB and PKA pathways
low molecular weight cyclin E upregulates enzymatic activity, subsequently increasing lipid droplet formation, thereby providing cells with essential building blocks to support growth
mRNA transcript levels decrease during normal macrophage differentiation from bone marrow precursors
overexpressed in many cancers. ACLY transcription is promoted by SREBP1
sterol regulatory element binding protein-1 up-regulates the enzyme at mRNA level via Akt signaling
the enzyme activity increases in the first 20 h during lipid accumulation
the enzyme is overexpressed in cancer cells
there are about 3fold increased levels of the enzyme in glioblastoma pseudopodia compared to unmigrated cells
transcription of genes aclA and aclB is repressed by growth on acetate or ethanol