EC Number |
General Information |
Reference |
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3.1.3.46 | malfunction |
knockdown of isoform PFKFB4 reduces tumor growth, glucose uptake and beta-D-fructose 2,6-bisphosphate and increases apoptosis |
730530 |
3.1.3.46 | metabolism |
analysis of glucokinase/6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase complex formation, binding and activation of GK by PFK-2/FBPase-2 in beta-cells is promoted by glucose, resulting in an enhancement of insulin secretion at stimulatory glucose concentrations, without affecting basal insulin secretion |
716226 |
3.1.3.46 | metabolism |
flux through phosphofructokinase-1 is controlled by the bifunctional enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 via production/degradation of fructose-2,6-bisphosphate, a potent allosteric activator of phosphofructokinase-1, as well as direct activation of glucokinase due to a protein-protein interaction |
730691 |
3.1.3.46 | more |
androgen stimulates glycolysis for de novo lipid synthesis by increasing the activities of hexokinase 2 and 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2, up-regulation of PFKFB2 expression is mediated by the direct binding of ligand-activated androgen receptor to the PFKFB2 promoter |
714090 |
3.1.3.46 | more |
bifunctional 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase |
713740 |
3.1.3.46 | physiological function |
both a PFKFB3 inhibitor or PFKFB3 silencing by siRNA suppress the basal and the H2O2-induced autophagy concomitantly with the inhibition of AMPK activity. Overexpression of wild-type PFKFB3 promotes H2O2-induced autophagy, but mutant K472/473A, which lost nuclear localizing property, inhibits the autophagic process. The K472/473A mutant stimulates more lactate production, and decreases the activity of AMPK compared to the wild-type |
751774 |
3.1.3.46 | physiological function |
fructose-2,6-bisphosphate synthesis by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 is required for the glycolytic response to hypoxia and tumor growth |
730530 |
3.1.3.46 | physiological function |
overexpression of microRNA miR-26b represses PFKFB3 mRNA and protein levels followed by modulation of the expression of glycolytic components such as LDHA, GLUT-1 and markers of invasion and cell cycle such as MMP-9, MMP-2, cyclin D1 and p27. The binding site for miR-26b is predicted in the 3'-untranslated region of the PFKFB3 gene |
751765 |
3.1.3.46 | physiological function |
PFK2/FBPase2 is most helpful to the glucose-sensing capacity of glucokinase in a fasted organism, or in the transition to threshold as glucose is elevated during feeding |
730691 |
3.1.3.46 | physiological function |
PFKFB2 has a critical role in glucose uptake and glucose-dependent lipid synthesis. Induction of de novo lipid synthesis by androgen requires the transcriptional up-regulation of HK2 and PFKFB2, and phosphorylation of PFKFB2 generated by the PI3K/Akt signalling pathway to supply the source for lipogenesis from glucose in prostate cancer cells |
714090 |