Schematic regulatory pathways for insulin- and diDCP-LA-PE-induced
Download scientific diagram | Schematic regulatory pathways for insulin- and diDCP-LA-PE-induced GLUT4 translocation. Insulin- or diDCP-LA-PE promotes GLUT4 translocation towards the cell surface through a PI3K/PDK1/Akt pathway and by activating PKCζ. PI3K, alternatively, activates the Rac1 GEF Tiam1, to activate Rac1. Activated Rac1, in turn, binds to and activate the Rac1 effector Dbs, a RhoA GEF, t activate RhoA. Activated RhoA activates the RhoA effector ROCK, leading to GLUT4 translocation towards the cell surface. from publication: Rac1 and ROCK are implicated in the cell surface delivery of GLUT4 under the control of the insulin signal mimetic diDCP-LA-PE | The phosphatidylethanolamine derivative 1,2-O-bis-[8-{2-(2-pentyl-cyclopropylmethyl)-cyclopropyl}-octanoyl]-sn-glycero-3-phosphatidylethanolamine (diDCP-LA-PE) promoted GLUT4 translocation to the cell surface in differentiated 3T3-L1-GLUT4myc adipocytes through a pathway | Insulin Signaling, Rocks and Phosphatidylinositol 3-Kinase | ResearchGate, the professional network for scientists.
Insulin Signaling Pathway
Abstracts from ATTD 2017 10th International Conference on Advanced
Long-Term Administration of Dehydroepiandrosterone Accelerates
Insulin-Mediated Stimulation of Protein Kinase Akt
Insulin Signaling - an overview
Structural basis of the mechanism and inhibition of a human
Adipocytokines & Insulin Signaling Interactive Pathway: R&D Systems
Metabolites as regulators of insulin sensitivity and metabolism
The pearl jubilee of microcin J25: thirty years of research on an
Roles for Insulin Receptor, PI3-Kinase, and Akt in Insulin
An expanded allosteric network in PTP1B by multitemperature
Gynura divaricata exerts hypoglycemic effects by regulating the
A stepwise activation model for the insulin receptor
Insulin Resistance: From Mechanisms to Therapeutic Strategies