EC Number   |
General Information |
Reference |
|---|
    2.7.1.1 | drug target |
given the absence of energy stores in this parasite and the key role of the Plasmodium falciparum hexose transporter, the pathway involving Plasmodium falciparum hexokinase and the bifunctional glucose-6-phosphate dehydrogenase 6-phosphogluconolactonase is promising as a pharmacotherapeutic target, particularly because Plasmodium falciparum hexokinase shows a low sequence identity with human hexokinases |
758656 |
| 2.7.1.1 | drug target |
glucokinase activators are being developed for the treatment of type 2 diabetes mellitus. Glucokinase activators have risks of hypoglycemia caused by over-activation of glucokinase in islet cells and dyslipidemia caused by over-activation of intrahepatic glucokinase. In the effort to mitigate risks of hypoglycemia and dyslipidemia while maintaining the promising efficacy of glucokinase activator. tert-Butyl (S)-2-(3-(4-(azetidine-1-carbonyl)phenoxy)-5-((1-methoxypropan-2-yl)oxy)benzamido)-6,7-dihydrothiazolo[5,4-c]pyridine-5(4H)-carboxylate shows a good balance between in vitro potency and enzyme kinetic parameters, and protects beta-cells from streptozotocin-induced apoptosis. Chronic treatment of this compound demonstrates its potent activity in regulation of glucose homeostasis and low risk of dyslipidemia with diabetic db/db mice in oral glucose tolerance test. Acute treatment of this compound does not induce hypoglycemia in C57BL/6J mice even at 200 mg/kg via oral administration |
759145 |
| 2.7.1.1 | drug target |
the enzyme is a promising target for cancer therapy |
758900 |
| 2.7.1.1 | drug target |
the identification of structural and biochemical differences between HK2 and other human hexokinase isozymes could potentially be used in the development of new anticancer therapies |
758942 |
| 2.7.1.1 | malfunction |
after silencing NtHXK1 using RNAi plants show stunted growth and leaf chlorosis |
723383 |
| 2.7.1.1 | malfunction |
an glucose-dependent root hair morphology is readily observed in Arabidopsis lines that overexpress HKL1 protein and in an HXK1-deficient line, gin2-1. Seedlings of these lines produce bulbous root hairs with an enlarged base after transfer from agar plates with normal medium to plates with 6% glucose. Seedling transfer to plates with 2% glucose plus 1-aminocyclopropane-1-carboxylic acid mimics the high-glucose effect in the HKL1 overexpression line but not in HXK1-deficient line gin2-1 |
723469 |
| 2.7.1.1 | malfunction |
D-allose activates AtABI5 expression in transgenic gin2 (mutant glucose-insensitive2-1 (gin2), which has a null mutation in the glucose sensor gene of AtHXK1) over-expressing wild-type AtHXK1 but not in gin2 over-expressing the catalytic mutant AtHXK1S177A, indicating that the D-allose phosphorylation by HXK to D-allose 6-phosphate (A6P) is the first step for the up-regulation of AtABI5 gene expression as well as D-allose-induced growth inhibition |
723503 |
| 2.7.1.1 | malfunction |
D-allose inhibits Arabidopsis growth but fails to trigger growth retardation in the AtHXK1 loss-of function mutant (gin2 mutant) |
723503 |
| 2.7.1.1 | malfunction |
defect in the activation of glucokinase is potential contributing factor to the dysregulation of hepatic glucose metabolism in type 2 diabetes |
702116 |
| 2.7.1.1 | malfunction |
DELTAFgHXK1 leads to inhibited vegetative growth and conidiation. DELTAFgHXK1 mutants lose virulence on wheat head and corn stigma. They show no change in sexual reproduction |
-, 759793 |
