scholarly journals Crk protein binds to PDGF receptor and insulin receptor substrate-1 with different modulating effects on PDGF- and insulin-dependent signaling pathways

Oncogene ◽  
1998 ◽  
Vol 16 (19) ◽  
pp. 2425-2434 ◽  
Author(s):  
Andrey Sorokin ◽  
Eleanor Reed ◽  
Naenna Nnkemere ◽  
Nickolai O Dulin ◽  
Joseph Schlessinger
Keyword(s):  
Insulin Receptor ◽  
Signaling Pathways ◽  
Insulin Receptor Substrate ◽  
Pdgf Receptor ◽  
Insulin Receptor Substrate 1 ◽  
Insulin Dependent

scholarly journals Reconstitution of Insulin Signaling Pathways in Rat 3Y1 Cells Lacking Insulin Receptor and Insulin Receptor Substrate-1

1998 ◽  
Vol 273 (39) ◽  
pp. 25347-25355 ◽  
Author(s):  
Takanobu Imanaka ◽  
Hideki Hayashi ◽  
Kazuhiro Kishi ◽  
Lihong Wang ◽  
Kazuo Ishii ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Signaling Pathways ◽  
Insulin Signaling ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1

scholarly journals Nutrients Suppress Phosphatidylinositol 3-Kinase/Akt Signaling via Raptor-Dependent mTOR-Mediated Insulin Receptor Substrate 1 Phosphorylation

2006 ◽  
Vol 26 (1) ◽  
pp. 63-76 ◽  
Author(s):  
Alexandros Tzatsos ◽  
Konstantin V. Kandror
Keyword(s):  
Insulin Receptor ◽  
Mammalian Target Of Rapamycin ◽  
Insulin Dependent Diabetes Mellitus ◽  
Akt Signaling ◽  
Pi3 Kinase ◽  
Dependent Diabetes Mellitus ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Insulin Dependent ◽  
Phosphatidylinositol 3

ABSTRACT Nutritional excess and/or obesity represent well-known predisposition factors for the development of non-insulin-dependent diabetes mellitus (NIDDM). However, molecular links between obesity and NIDDM are only beginning to emerge. Here, we demonstrate that nutrients suppress phosphatidylinositol 3 (PI3)-kinase/Akt signaling via Raptor-dependent mTOR (mammalian target of rapamycin)-mediated phosphorylation of insulin receptor substrate 1 (IRS-1). Raptor directly binds to and serves as a scaffold for mTOR-mediated phosphorylation of IRS-1 on Ser636/639. These serines lie close to the Y632MPM motif that is implicated in the binding of p85α/p110α PI3-kinase to IRS-1 upon insulin stimulation. Phosphomimicking mutations of these serines block insulin-stimulated activation of IRS-1-associated PI3-kinase. Knockdown of Raptor as well as activators of the LKB1/AMPK pathway, such as the widely used antidiabetic compound metformin, suppress IRS-1 Ser636/639 phosphorylation and reverse mTOR-mediated inhibition on PI3-kinase/Akt signaling. Thus, diabetes-related hyperglycemia hyperactivates the mTOR pathway and may lead to insulin resistance due to suppression of IRS-1-dependent PI3-kinase/Akt signaling.

scholarly journals Insulin receptor substrate-1 variants in non-insulin-dependent diabetes.

1994 ◽  
Vol 94 (3) ◽  
pp. 1141-1146 ◽  
Author(s):  
M Laakso ◽  
M Malkki ◽  
P Kekäläinen ◽  
J Kuusisto ◽  
S S Deeb
Keyword(s):  
Insulin Receptor ◽  
Insulin Dependent Diabetes ◽  
Insulin Receptor Substrate ◽  
Insulin Receptor Substrate 1 ◽  
Insulin Dependent
Sign in / Sign up

Export Citation Format

Share Document