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Literature summary for 2.7.1.28 extracted from

  • Liu, L.; Li, T.; Liao, Y.; Wang, Y.; Gao, Y.; Hu, H.; Huang, H.; Wu, F.; Chen, Y.G.; Xu, S.; Fu, S.
    Triose kinase controls the lipogenic potential of fructose and dietary tolerance (2020), Cell Metab., 32, 1-14 .
    View publication on PubMed
Search for more literature for 2.7.1.28

Protein Variants

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/ Products (Substrates)

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

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

Source Tissue Comment Organism Textmining
hepatocyte primary Mus musculus
-
liver
-
 Homo sapiens
-
liver
-
 Mus musculus
-

Substrates and Products (Substrate)

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

Synonyms Comment Organism
TKFC
-
 Homo sapiens
TKFC
-
 Mus musculus
triose kinase
-
 Homo sapiens
triose kinase
-
 Mus musculus

General Information

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