Protein Variants | Comment | Organism |
---|---|---|
additional information | construction of Tk-null models to study the biological significance of the GA branch point in fructose metabolism, overview | Homo sapiens |
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 | Mus musculus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + D-glyceraldehyde | Homo sapiens | - |
ADP + D-glyceraldehyde 3-phosphate | - |
? | |
ATP + D-glyceraldehyde | Mus musculus | - |
ADP + D-glyceraldehyde 3-phosphate | - |
? | |
ATP + D-glyceraldehyde | Mus musculus C57BL/6J | - |
ADP + D-glyceraldehyde 3-phosphate | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q3LXA3 | bifunctional triokinase/FMN cyclase | - |
Mus musculus | Q8VC30 | bifunctional triokinase/FMN cyclase | - |
Mus musculus C57BL/6J | Q8VC30 | bifunctional triokinase/FMN cyclase | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
hepatocyte | primary | Mus musculus | - |
liver | - |
Homo sapiens | - |
liver | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
ATP + D-glyceraldehyde | - |
Homo sapiens | ADP + D-glyceraldehyde 3-phosphate | - |
? | |
ATP + D-glyceraldehyde | - |
Mus musculus | ADP + D-glyceraldehyde 3-phosphate | - |
? | |
ATP + D-glyceraldehyde | - |
Mus musculus C57BL/6J | ADP + D-glyceraldehyde 3-phosphate | - |
? |
Synonyms | Comment | Organism |
---|---|---|
TKFC | - |
Homo sapiens |
TKFC | - |
Mus musculus |
triose kinase | - |
Homo sapiens |
triose kinase | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
evolution | triose kinase polymorphism demarcates the routes of human migration out of Africa. A nonsynonymous TK allele (rs2260655_A) segregated during human migration out of Africa behaves as TK null for its inability to rescue fructose toxicity and increase hepatic triglyceride accumulation | Homo sapiens |
malfunction | triose kinase deficiency causes oxidative stress and dietary fructose intolerance. In the absence of TK, fructose oxidation is accelerated through the activation of aldehyde dehydrogenase (ALDH) and serine biosynthesis, accompanied by increased oxidative stress and fructose aversion. A nonsynonymous TK allele (rs2260655_A) segregated behaves as TK null for its inability to rescue fructose toxicity and increase hepatic triglyceride accumulation | Homo sapiens |
malfunction | triose kinase deficiency causes oxidative stress and dietary fructose intolerance. In the absence of TK, fructose oxidation is accelerated through the activation of aldehyde dehydrogenase (ALDH) and serine biosynthesis, accompanied by increased oxidative stress and fructose aversion. A nonsynonymous TK allele (rs2260655_A) segregated behaves as TK null for its inability to rescue fructose toxicity and increase hepatic triglyceride accumulation. Deletion of Tk nearly doubles the rate of fructose oxidation, but not the rate of lactate secretion providing an initial indication that TK deficiency may differentially modulate fructose metabolism downstream of glyceraldehyde. Enzyme TK deficiency sensitizes cells to fructose toxicity. TK-deficient mice develop fructose avoidance. TK deficiency reduces hepatic triglyceride accumulation | Mus musculus |
metabolism | the dual association of fructose with metabolic syndrome and intolerance is controlled by triose kinase (TK) through the metabolic bifurcation of fructose toward oxidative versus lipogenic routes. Fructose is catabolized at a much higher rate than glucose, and triose kinase (TK) couples fructolysis with lipogenesis metabolically and transcriptionally. Triose kinase controls the fate of fructose metabolism glyceraldehyde (GA) represents the only branch point in fructose metabolism | Homo sapiens |
metabolism | the dual association of fructose with metabolic syndrome and intolerance is controlled by triose kinase (TK) through the metabolic bifurcation of fructose toward oxidative versus lipogenic routes. Fructose is catabolized at a much higher rate than glucose, and triose kinase (TK) couples fructolysis with lipogenesis metabolically and transcriptionally. Triose kinase controls the fate of fructose metabolism glyceraldehyde (GA) represents the only branch point in fructose metabolism | Mus musculus |
physiological function | triose kinase (TK) constrains fructose oxidation in favor of lipogenic metabolism. Hyperglycemia activates fructolysis through TK to stimulate hepatic lipogenesis. The dual association of fructose with metabolic syndrome and intolerance is controlled by triose kinase (TK) through the metabolic bifurcation of fructose toward oxidative versus lipogenic routes. TK is also required by the endogenous fructolysis pathway to drive lipogenesis and hepatic triglyceride accumulation under high-fat diet and leptin-deficient conditions | Homo sapiens |
physiological function | triose kinase (TK) constrains fructose oxidation in favor of lipogenic metabolism. Hyperglycemia activates fructolysis through TK to stimulate hepatic lipogenesis. The dual association of fructose with metabolic syndrome and intolerance is controlled by triose kinase (TK) through the metabolic bifurcation of fructose toward oxidative versus lipogenic routes. TK is also required by the endogenous fructolysis pathway to drive lipogenesis and hepatic triglyceride accumulation under high-fat diet and leptin-deficient conditions | Mus musculus |