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Figure 2 | Theoretical Biology and Medical Modelling

Figure 2

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

Figure 2

Schematic representation of metabolic Insulin signaling pathway used for the steady state analysis. Nomenclature: I, Insulin; X, unbound surface insulin receptor; XI, unphosphorylated once-bound surface receptor; XIP, phosphorylated once-bound surface receptor; XI2P, phosphorylated twice-bound surface receptor; Xi represents intracellular receptor pool; XIPi and XI2Pi are internalized form of XIP and XI2P; phosphatase PTP catalyzes the dephosphorylation of AP, XIP, XIPi and XI2Pi. A, unphosphorylated IRS-1; AP, phosphorylated IRS-1; B, inactive PI3-kinase; APB, phosphorylated IRS-1 and PI3-kinase complex; CP3, lipid PI[3,4,5]P3; CP2, lipid PI[4,5]P2; CP2', lipid PI[3,4]P2; phosphatase SHIP2 catalyzes dephosphorylation of CP3 to form CP2', phosphatase PTEN catalyzes dephosphorylation of CP3 to form CP2; F, inactive Akt and PKC-ς; FP, phosphorylated Akt and PKC-ς; E8 dephosphorylates FP; E6 phosphorylates CP2' to form CP3; FP activates GLUT4 from intracellular location to plasma membrane. GC and GM represent GLUT4 in cytoplasm and on plasma membrane respectively. Kd1 to Kd3 are dissociation constants; Kd4 and Kd5 are distribution coefficients; Kmr, Km, Km1to Km8 are Michaelis-Menten constants; k, kp, kd, ks, k0, k1 to k13 are reaction rates as shown in the figure.

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