Gene interactions and pathways from curated databases and text-mining

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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