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Figure 1 | Theoretical Biology and Medical Modelling

Figure 1

From: A steady state analysis indicates that negative feedback regulation of PTP1B by Akt elicits bistability in insulin-stimulated GLUT4 translocation

Figure 1

Simplified representation of molecular mechanism involved in insulin signaling pathway that regulates glucose transporter (GLUT4) translocation to cell membrane. Some of the details like, other isoforms of insulin receptor substrate and multiphosphorylation of insulin receptor substrate are not shown here. Nomenclature: GLUT4: Glucose-transporter isoform 4; IRS-1: Insulin receptor substrate-1; PI3K: Phosphatidylinositol-3-kinase; PI (3, 4, 5) P3: Phosphatidylinositol (PI)-3, 4, 5-tiphosphate; PDK1: phosphosinsositide-dependent kinase 1; Akt: Protein kinase Akt or protein kinase B (PKB); PKC: Protein kinase C-Ï‚; PTP1B: Protein tyrosine phosphatase 1B; PTEN: 3' lipid phosphatase; SHIP2: 5' lipid phosphatase; Detailed description of signaling events are given in the methods section. Letter 'P' indicates phosphorylated species.

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Theoretical Biology and Medical Modelling

ISSN: 1742-4682