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Literature summary for 2.7.1.3 extracted from

  • Li, X.; Qian, X.; Peng, L.X.; Jiang, Y.; Hawke, D.H.; Zheng, Y.; Xia, Y.; Lee, J.H.; Cote, G.; Wang, H.; Wang, L.; Qian, C.N.; Lu, Z.
    A splicing switch from ketohexokinase-C to ketohexokinase-A drives hepatocellular carcinomaformation (2016), Nat. Cell Biol., 18, 561-571.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine compared with normal hepatocytes, hepatocellular carcinoma cells markedly reduce the rate of fructose metabolism and the level of reactive oxygen species, as a result of a c-Myc-dependent and heterogeneous nuclear ribonucleoprotein H1- and H2-mediated switch from expression of the high-activity fructokinase KHK-C to the low-activity KHK-A isoform. KHK-A acts as a protein kinase, phosphorylating and activating phosphoribosyl pyrophosphate synthetase PRPS1. c-Myc, hnRNPH1/2 and KHK-A expression levels and PRPS1 Thr225 phosphorylation levels correlate with each other in hepatocellular carcinoma specimens and are associated with poor prognosis for hepatocellular carcinoma Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
HEP-3B cell
-
Homo sapiens
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Huh-7 cell hepatocellular carcinoma cell Homo sapiens
-

Synonyms

Synonyms Comment Organism
Khk-A
-
Homo sapiens
Khk-C
-
Homo sapiens