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Rat Ketone Body Metabolic Process

Also showing Mouse Ketone Body Metabolic Process, Human Ketone Body Metabolic Process

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: Mitochondrial acetyl-coenzyme A (CoA) acetyltransferase 1 (ACAT1) plays a pivotal role in ketogenesis and branched chain amino acid metabolism (1-3). Research studies have demonstrated that ACAT1 also plays a key role in carbohydrate metabolism of tumor cells by directly acetylating and inhibiting the activity of the pyruvate dehydrogenase complex (PDH) and PDH phosphatase, which leads to decreased carbon flux through PDH and increased glycolysis (4,5). Mechanistically, it has been shown that numerous oncogenic tyrosine kinases directly phosphorylate ACAT1 at Y407, which promotes tetramerization and stabilization of the active enzyme in order to drive glycolysis and tumor growth (5).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

Background: Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS2) generates hydroxymethylglutaryl-CoA (HMG-CoA) from acetyl-CoA and acetoacetyl-CoA, a rate-limiting step in ketogenesis (1). Starvation or a high-fat and low-carbohydrate diet increases the levels of hepatic FGF21, which in turn up-regulates HMGCS2 expression (2). Furthermore, mTORC1 inhibition was shown to be required for the increase of HMGCS2 expression mediated by PPARα in response to fasting (3). In addition, studies on mice lacking HMGCS2 suggest that ketogenesis plays a role in the prevention of diet-induced fatty liver injury and hyperglycemia (4).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Western Blotting

Background: Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS2) generates hydroxymethylglutaryl-CoA (HMG-CoA) from acetyl-CoA and acetoacetyl-CoA, a rate-limiting step in ketogenesis (1). Starvation or a high-fat and low-carbohydrate diet increases the levels of hepatic FGF21, which in turn up-regulates HMGCS2 expression (2). Furthermore, mTORC1 inhibition was shown to be required for the increase of HMGCS2 expression mediated by PPARα in response to fasting (3). In addition, studies on mice lacking HMGCS2 suggest that ketogenesis plays a role in the prevention of diet-induced fatty liver injury and hyperglycemia (4).