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KHK encodes ketohexokinase that catalyzes conversion of fructose to fructose-1-phosphate. Additionally we are shipping Ketohexokinase Antibodies (110) and Ketohexokinase Proteins (18) and many more products for this protein.
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Feedforward upregulation of fructolytic and gluconeogenic enzymes specifically requires GLUT5 (show SLC2A5 ELISA Kits) and KHK and may proactively enhance the intestine's ability to process anticipated increases in dietary fructose concentrations.
Significant levels of blood fructose are maintained independent of dietary fructose, KHK, and GLUT5 (show SLC2A5 ELISA Kits), probably by endogenous synthesis of fructose.
myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1alpha (HIF1alpha (show HIF1A ELISA Kits)) activation of SF3B1 (show SF3B1 ELISA Kits) and SF3B1 (show SF3B1 ELISA Kits)-mediated splice switching of KHK-A to KHK-C
Fructokinase-knockout mice with delayed hydration were protected from renal injury. Thus, recurrent dehydration can induce renal injury via a fructokinase-dependent mechanism, likely from the generation of endogenous fructose via the polyol pathway.
This study demonstrates that blocking KHK and redirecting fructose metabolism to alternative pathways is an effective way to prevent visceral obesity and insulin (show INS ELISA Kits) resistance induced by high fructose, a widespread component of Western diets.
These studies identify fructokinase as a novel mediator of diabetic nephropathy and document a novel role for endogenous fructose production, or fructoneogenesis, in driving renal disease.
High-fat and high-sucrose (western) diet induces steatohepatitis that is dependent on fructokinase.
Fructose-induced metabolic syndrome is prevented in mice lacking both fructokinase B and A but is exacerbated in mice lacking fructokinase A.
These studies are the first demonstration that neither Khk isoform is required for normal growth and development.
myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1alpha (HIF1alpha (show HIF1A ELISA Kits)) activation of SF3B1 and SF3B1-mediated splice switching of KHK-A to KHK-C
This study determined if single nucleotide polymorphisms in genes involved in fructose transport,SLC2A2 (show SLC2A2 ELISA Kits) and SLC2A5 (show SLC2A5 ELISA Kits) and metabolism, etohexokinase affect inter-individual variability in metabolic phenotypes.
In human hepatocytes uric acid up-regulates KHK expression thus leading to the amplification of the lipogenic effects of fructose.
ketohexokinase-A serves an unknown physiologic function that remains intact in essential fructosuria.
The expression of ketohexokinase is diminished in human clear cell type of renal cell carcinoma
Ketohexokinase-dependent metabolism of fructose induces proinflammatory mediators in proximal tubular cells.
The structure of the KHK-A ternary complex revealed an active site with fructose & the ATP analogue in positions ready for phosphorylation. The effects of the pathogenic mutations Gly40Arg & Ala43Thr have been modelled in the context of the KHK structure.
This gene encodes ketohexokinase that catalyzes conversion of fructose to fructose-1-phosphate. The product of this gene is the first enzyme with a specialized pathway that catabolizes dietary fructose. Alternatively spliced transcript variants encoding different isoforms have been identified.
, hepatic fructokinase