◀ Back to IGF1
IGF1 — PTPN11
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Integrins in angiogenesis:
IGF-1R heterotetramer/IGF1/IRS1/Shp2 complex (IGF1R-IGF1-IRS1-PTPN11)
→
SHP2 (PTPN11)
(modification, collaborate)
Kuemmerle et al., Am J Physiol Gastrointest Liver Physiol 2006
Evidence: assay, physical interaction
-
NCI Pathway Database Integrins in angiogenesis:
IGF-1R heterotetramer/IGF1/IRS1/Shp2 complex (IGF1R-IGF1-IRS1-PTPN11)
→
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
(modification, collaborate)
Kuemmerle et al., Am J Physiol Gastrointest Liver Physiol 2006
Evidence: assay, physical interaction
-
NCI Pathway Database Integrins in angiogenesis:
SHP2 (PTPN11)
→
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
(modification, collaborate)
Kuemmerle et al., Am J Physiol Gastrointest Liver Physiol 2006
Evidence: assay, physical interaction
-
NCI Pathway Database IGF1 pathway:
IGF-1R heterotetramer/IGF1/IRS1/Shp2 complex (IGF1R-IGF1-IRS1-PTPN11)
→
SHP2 (PTPN11)
(modification, collaborate)
Amoui et al., J Endocrinol 2001*
Evidence: assay, physical interaction
-
NCI Pathway Database IGF1 pathway:
IGF-1R heterotetramer/IGF1/IRS1/Shp2 complex (IGF1R-IGF1-IRS1-PTPN11)
→
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
(modification, collaborate)
Amoui et al., J Endocrinol 2001*
Evidence: assay, physical interaction
-
NCI Pathway Database IGF1 pathway:
SHP2 (PTPN11)
→
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
(modification, collaborate)
Amoui et al., J Endocrinol 2001*
Evidence: assay, physical interaction
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