the binding of ATP to the fructose 2,6-bisphosphatase domain of chicken liver 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase leads to activation of enzyme, but no activation of rat liver enzyme
the binding of ATP to the fructose 2,6-bisphosphatase domain of chicken liver 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase leads to activation of enzyme, but no activation of rat liver enzyme
activation of transfected heart enzyme in human embryonic kidney 293 cells by inducing the phosphorylation of Ser466 and Ser483, activation is mediated by 3-phosphoinositide-dependent kinase-1, protein kinase B is in vivo not essential, activation is sensitive to LY294002 and wortmannin and insensitive to rapaycin and PD98059
stimulates glycolysis in the heart by increasing glucose transport and activating H-PFK2 by phosphorylating Ser466 and Ser483 through protein kinase B within the C-terminal regulatory domain. Phosphorylation of Ser466 or Thr475 by protein kinase C does not change the enzyme activity. Phosphorylation at Ser84 possibly counteracts the effects of phosphorylation at the activating C-terminal sites
amino acids increase beta-D-fructose 2,6-bisphosphate concentration in HeLa and in MCF-7 human cells, molecular mechanisms involved differ from those observed with insulin. Only essential amino acids without glutamine are required to activate the PI3K/mTORC2 and p38/MAPKAPK-2 pathways and to increase the beta-D-fructose 2,6-bisphosphate concentration. The observed effects in signaling and metabolism are produced by a mixture of essential amino acids
amino acids increase beta-D-fructose 2,6-bisphosphate concentration in HeLa and in MCF-7 human cells, molecular mechanisms involved differ from those observed with insulin. Only essential amino acids without glutamine are required to activate the PI3K/mTORC2 and p38/MAPKAPK-2 pathways and to increase the beta-D-fructose 2,6-bisphosphate concentration. The observed effects in signaling and metabolism are produced by a mixture of essential amino acids
amino acids increase beta-D-fructose 2,6-bisphosphate concentration in primary cardiomyocytes, molecular mechanisms involved differ from those observed with insulin. Only essential amino acids without glutamine are required to activate the PI3K/mTORC2 and p38/MAPKAPK-2 pathways and to increase the beta-D-fructose 2,6-bisphosphate concentration. The observed effects in signaling and metabolism are produced by a mixture of essential amino acids