2.7.1.28: triokinase
This is an abbreviated version!
For detailed information about triokinase, go to the full flat file.
Word Map on EC 2.7.1.28
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2.7.1.28
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fructose
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dihydroxyacetone
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fructokinase
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ketohexokinase
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gluconeogenesis
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glycerate
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fructolysis
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d-glyceric
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fructose-1-phosphate
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fructose-metabolizing
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gluconeogenic
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malabsorption
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glucose-6-phosphatase
- 2.7.1.28
- fructose
- dihydroxyacetone
- fructokinase
- ketohexokinase
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gluconeogenesis
- glycerate
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fructolysis
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d-glyceric
- fructose-1-phosphate
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fructose-metabolizing
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gluconeogenic
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malabsorption
- glucose-6-phosphatase
Reaction
Synonyms
D-triokinase, dAK, hTKFC, kinase, trio (phosphorylating), TKFC, triokinase/FMN cyclase, triose kinase
ECTree
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Engineering
Engineering on EC 2.7.1.28 - triokinase
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G445S
naturally occuring mutation and site-directed mutagenesis, almost inactive mutant
R543I
naturally occuring mutation and site-directed mutagenesis, almost inactive mutant
additional information
analysis of bi-allelic TKFC variants from two families, DNA sequence determinations and analysis, and phenotypic analyses of genetic variants, detailed overview. Utility of genome sequencing and data sharing in the identification of an inborn error of metabolism
additional information
construction of Tk-null models to study the biological significance of the GA branch point in fructose metabolism, overview
additional information
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construction of Tk-null models to study the biological significance of the GA branch point in fructose metabolism, overview
additional information
construction of TK-null models to study the biological significance of the GA branch point in fructose metabolism. Deletion of TK nearly doubles the rate of fructose oxidation, but not the rate of lactate secretion. Analysis of glyceraldehyde metabolism in wild-type and TK knockout primary hepatocytes in minimal medium, overview. Enzyme TK deficiency sensitizes cells to fructose toxicity. TK-deficient mice develop fructose avoidance. Tk deficiency reduces hepatic triglyceride accumulation
additional information
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construction of TK-null models to study the biological significance of the GA branch point in fructose metabolism. Deletion of TK nearly doubles the rate of fructose oxidation, but not the rate of lactate secretion. Analysis of glyceraldehyde metabolism in wild-type and TK knockout primary hepatocytes in minimal medium, overview. Enzyme TK deficiency sensitizes cells to fructose toxicity. TK-deficient mice develop fructose avoidance. Tk deficiency reduces hepatic triglyceride accumulation
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