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.

Schematic regulatory pathways for insulin- and diDCP-LA-PE-induced

The regulatory role of insulin in energy metabolism and leukocyte

Insulin-Mediated Stimulation of Protein Kinase Akt

Long-Term Administration of Dehydroepiandrosterone Accelerates

An expanded allosteric network in PTP1B by multitemperature

Mechanisms for Insulin Resistance: Common Threads and Missing

Roles for Insulin Receptor, PI3-Kinase, and Akt in Insulin

PI3 kinase directly phosphorylates Akt1/2 at Ser473/474 in the

Abstracts from ATTD 2017 10th International Conference on Advanced