Gene interactions and pathways from curated databases and text-mining

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IGF1 — PTPN11

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Mañes et al., Mol Cell Biol 1999 (Neoplasm Invasiveness) : On the other hand, IGF-I promotes the association of insulin receptor substrate 1 with the focal adhesion kinase ( FAK ), paxillin, and the tyrosine phosphatase SHP-2 , resulting in FAK and paxillin dephosphorylation
Maile et al., Mol Biol Cell 2003 : We undertook these studies to determine whether this interaction controlled SHPS-1 phosphorylation and/or SHP-2 recruitment and thereby regulated IGF-I signaling ... Disruption of IAP-SHPS-1 binding, by using an IAP monoclonal antibody or cells expressing mutant forms of IAP that did not bind to SHPS-1, inhibited IGF-I stimulated SHPS-1 phosphorylation and SHP-2 recruitment
Maile et al., Circ Res 2003 : Ligand occupancy of SHPS-1 with IAP is required for the recruitment and transfer of SHP-2 and subsequent signaling in response to IGF-I
Kwon et al., Endocrinology 2006 : However, the mechanism by which SHP-2 phosphatase activity or the recruitment of SHP-2 to other signaling molecules contributes to IGF-I stimulated PI-3 kinase activation has not been determined ... Similarly in cells expressing native SHP-2, IGF-I induced SHP-2 binding to p85, whereas in cells expressing SHP-2/C459S, there was no increase
Lieskovska et al., J Biol Chem 2006 (MAP Kinase Signaling System) : IGF-I induced both Src/SHP-2 and Src/SHPS-1 association
Radhakrishnan et al., J Biol Chem 2010 (MAP Kinase Signaling System) : These cultures showed reduced SHPS-1 phosphorylation, transfer of SHP-2 to SHPS-1, and impaired Shc and MAPK phosphorylation and cell proliferation in response to IGF-I
Shen et al., Cell Mol Life Sci 2010 (MAP Kinase Signaling System) : In vascular smooth muscle cells, IGF-I stimulates SHPS-1/SHP2/Src complex formation which is required for IGF-I stimulated cell proliferation
Xi et al., Endocrinology 2010 (Hyperglycemia) : Mechanistic studies showed that knockdown of p66shc enhanced IGF-I stimulated SHPS-1/p85, p85/SHP-2 , and p85/Grb2 association, all of which are required for PI-3 kinase/AKT activation
De Rocca Serra-Nédélec et al., Proc Natl Acad Sci U S A 2012 (Noonan Syndrome) : Noonan syndrome causing SHP2 mutants inhibit insulin-like growth factor 1 release via growth hormone induced ERK hyperactivation, which contributes to short stature ... Conversely, inhibition of SHP2 expression in growth hormone (GH)-responsive cell lines results in increased IGF-1 release upon GH stimulation ... In conclusion, NS-causing SHP2 mutants inhibit GH-induced IGF-1 release through RAS/ERK1/2 hyperactivation, a mechanism that could contribute to growth retardation
Crossland et al., Am J Physiol Endocrinol Metab 2013 : However, binding of FAK to TSC2 or its phosphatase Shp-2 was not affected by IGF-I or cell phenotype