EC Number   |
General Information |
Reference |
|---|
   2.7.1.3 | drug target |
ketohexokinase may be a therapeutic target. Complete knockout of all ketohexokinase isoforms prevents fructose-induced disease. In contrast, selective knockout of the ubiquitous, low-activity KHK-A isoform exacerbates fructose-induced disease, possibly by increasing flux through the KHK-C isoform expressed in key metabolic tissues, like liver |
760221 |
| 2.7.1.3 | malfunction |
functionally, knockdown of ketohexokinase can significantly inhibit cell proliferation and migration of glioma cells in fructose medium |
758732 |
| 2.7.1.3 | malfunction |
two mouse knockout models are generated: one strain is selectively deficient in peripheral Khk-A, while the second strain lacks activity of both Khk-A and Khk-C. Both homozygous knockout mice are healthy and fertile and display minimal biochemical abnormalities under basal dietary conditions |
723348 |
| 2.7.1.3 | metabolism |
fructose increases de novo lipogenesis through the efficient and uninhibited action of ketohexokinase and aldolase B, which yields substrates for fatty-acid synthesis. Chronic fructose consumption further enhances the capacity for hepatic fructose metabolism via activation of several key transcription factors (i.e. SREBP1c and ChREBP), which augment expression of lipogenic enzymes, increasing lipogenesis, further compounding hypertriglyceridemia, and hepatic steatosis. Hepatic insulin resistance develops from diacylglycerol-PKCe mediated impairment of insulin signaling and possibly additional mechanisms |
760221 |
| 2.7.1.3 | metabolism |
fructose metabolism by ketohexokinase increases sodium hydrogen exchanger activity in renal proximal tubular cells via decreased intracellular cAMP level, resulting in increased renal sodium reabsorption and blood pressure in mice |
759646 |
| 2.7.1.3 | metabolism |
fructose-driven glycolytic respiration in Heterocephalus glaber tissues avoids feedback inhibition of glycolysis via phosphofructokinase, allowing continued glycolytic flux independent of cellular energy status and supporting viability |
760194 |
| 2.7.1.3 | metabolism |
increased fructose consumption and its subsequent metabolism are implicated in hepatic steatosis, dyslipidemia, obesity, and insulin resistance |
759602 |
| 2.7.1.3 | metabolism |
ketohexokinase overexpression is significantly correlated with tumor malignancy and poor survival of glioma patients |
758732 |
| 2.7.1.3 | metabolism |
ketohexokinase-dependent induction by fructose of lipogenic gene expression in small intestine |
759645 |
| 2.7.1.3 | metabolism |
key enzyme involved in fructose catabolism |
758732 |
