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The protein encoded by CS is a Krebs tricarboxylic acid cycle enzyme that catalyzes the synthesis of citrate from oxaloacetate and acetyl coenzyme A. Additionally we are shipping Citrate Synthase Antibodies (99) and Citrate Synthase Proteins (15) and many more products for this protein.
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Liu, Vachharajani, Millet, Bharadwaj, Molina, McCall: Sequential actions of SIRT1-RELB-SIRT3 coordinate nuclear-mitochondrial communication during immunometabolic adaptation to acute inflammation and sepsis. in The Journal of biological chemistry 2015
METTL12 methylates CS on Lys-395, which is localized in the CS active site. Interestingly, the METTL12-mediated methylation inhibited CS activity and was blocked by the CS substrate oxaloacetate.
Data suggest that METTL12, localized in mitochondrial matrix, modifies/methylates Lys368 of citrate synthase in external surface region close to its catalytic site; addition/removal of methylation has no effect on citrate synthase activity; Lys368 occurs in highly conserved sequence of amino acid residues of citrate synthase. (METTL12 = methyltransferase-like protein 12)
Data suggest that downregulation of citrate synthase (CS) expression in 293T cells leads to low level of ATP production, excessive superoxide formation and cell apoptosis, which implies a possible mechanism for hearing loss in A/J mice.
Hence, we conclude that SIRT3 (show SIRT3 ELISA Kits) exhibits neuroprotection via deacetylating and increasing mitochondrial enzyme activities.
The citrate synthase knockdown cells exhibited severe defects in respiratory activity and marked decreases in ATP production, but great increases in glycolytic metabolism.
Citrate synthase (CS) is a direct RORalpha target gene and one mechanism by which RORalpha regulates lipid metabolism is via regulation of CS expression.
It is likely that enhanced citrate synthase activity contributes to the conversion of glucose to lipids in pancreatic cancer providing substrate for membrane lipids synthesis.
These results provide an important basis for the study of mitochondrial dysfunction due to aberrant CSa trafficking.
The CS activity decreased in the infarcted tissue of wild-type (WT) mice at day 1 post-MI (p<0.05), but this was not observed in the MMP-9 (show MMP9 ELISA Kits) null mice, suggesting that MMP-9 (show MMP9 ELISA Kits) deletion helps to maintain the mitochondrial activity post-MI
Multiple lines of evidence implicate this missense mutation (H55N) as the underlying cause of ahl4-related hearing loss, likely through its effects on mitochondrial adenosine trisphosphate (ATP) and free radical production in cochlear hair cells.
CS and SERCA (show ATP2A3 ELISA Kits) activities were significantly higher in the pubococcygeus (Pc) compared with the ischiocavernosus/bulbospongiosus (Ic/Bs) pelvic floor muscles, whereas the ChAT activity of the Ic/Bs was higher than that of the Pc muscle.
The protein encoded by this gene is a Krebs tricarboxylic acid cycle enzyme that catalyzes the synthesis of citrate from oxaloacetate and acetyl coenzyme A. The enzyme is found in nearly all cells capable of oxidative metablism. This protein is nuclear encoded and transported into the mitochondrial matrix, where the mature form is found.
citrate synthase, mitochondrial
, Citrate synthase, mitochondrial