◀ Back to IGF2
IGF2 — INSR
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
INSR
→
Complex of IGF2-INSR
(increases, IGF2/INSR Activity)
Evidence: IGFs can also bind and activate the insulin receptor
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Sciacca et al., Oncogene 1999
(Breast Neoplasms) :
Insulin receptor activation by
IGF-II in breast cancers : evidence for a new autocrine/paracrine mechanism
Denley et al., Horm Metab Res 2003
(Diabetes Mellitus...) :
Activation of the exon 11-
insulin receptor by
IGF-II and insulin results in mitogenic effects and a potentiation of the cancer phenotype
Denley et al., Mol Cell Biol 2007
:
Differential
activation of
insulin receptor substrates 1 and 2 by
insulin-like growth factor activated insulin receptors
Diaz et al., Mol Hum Reprod 2007
(Choriocarcinoma...) :
IGF-II effects involve the activation of the
InsR while IGF-I uses the IGF-IR
Barnes et al., Clin Cancer Res 2007
(Head and Neck Neoplasms) :
Pretreatment of serum starved 183A or TU159 SCCHN cell lines with A12 ( 10 microg/mL ) blocked
IGF stimulated activation of IGF-IR,
insulin receptor substrate (IRS)-1 and IRS-2, mitogen activated protein kinase, and phosphatidylinositol 3-kinase
Hasslacher et al., Exp Clin Endocrinol Diabetes 2010
(Diabetic Nephropathies) :
This might be due to a stimulating effect of insulin analogs on erythropoiesis via
IGF receptor or a sustained
activation of the
insulin receptor
Morcavallo et al., J Biol Chem 2012
:
Insulin and
insulin-like growth factor II differentially
regulate endocytic sorting and stability of
insulin receptor isoform A
Mottola et al., J Biol Chem 1984
(Carcinoma, Ehrlich Tumor...) :
Rather, at least in H-35 cells, the
insulin receptor appears to
mediate the effects of
IGF II on cell growth
Foley et al., J Biol Chem 1982
(Chondrosarcoma...) :
Similarly, the
anti-insulin receptor IgG only partially
inhibited the binding of 125I-IGF-I and
125I-IGF-II while completely blocking the binding of 125I-insulin
Takata et al., Metabolism 1996
:
These results suggest that the Asp 1048 IR causes a dominant negative effect on
IGF-IR in transmitting signals to Shc and MAP kinase activation, which leads to decreased IGF-I stimulated DNA synthesis, and that the kinase-defective
insulin receptor does not
affect IGF-I stimulated IRS-I phosphorylation, which leads to the normal IGF-I stimulated glycogen synthesis