Nanopublications LDF server

Matches in Nanopublications for { ?s ?p "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" ?g. }

• _2 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _2 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _4 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _5 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _3 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _4 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _5 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _2 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _4 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _2 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _6 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _3 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _4 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _4 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _4 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.
• _6 value "Inhibition of PI3-kinase activity using a dominant negative mutant (30), or pharmacological agents such as wortmannin or LY294002 (31), abolishes insulin stimulated glucose uptake and inhibits GLUT4 vesicle translocation to the plasma membrane. Many other cellular effects of insulin, such as antilipolysis, activation of fatty acid synthesis, acetyl CoA-carboxylase, glycogen synthase, Akt phosphorylation, glycogen synthase kinase 3b inactivation, and stimulation of protein synthesis and DNA synthesis, are also inhibited by PI3- kinase suppression PIP3, rather than PIP2, is the major mediator of PI3- kinase dependent biological actions of insulin" provenance.