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IGF2 — SHC1
Pathways - manually collected, often from reviews:
-
Reactome Reaction:
SHC1
→
IGF2
(reaction)
Hernández-Sánchez et al., J Biol Chem 1995*, Tartare-Deckert et al., J Biol Chem 1995*, Giorgetti et al., Eur J Biochem 1994*, Kim et al., J Biol Chem 1998
-
Reactome Reaction:
SHC1
→
IGF2
(indirect_complex)
Hernández-Sánchez et al., J Biol Chem 1995*, Tartare-Deckert et al., J Biol Chem 1995*, Giorgetti et al., Eur J Biochem 1994*, Kim et al., J Biol Chem 1998
-
Reactome Reaction:
IGF2
→
SHC1
(indirect_complex)
Hernández-Sánchez et al., J Biol Chem 1995*, Tartare-Deckert et al., J Biol Chem 1995*, Giorgetti et al., Eur J Biochem 1994*, Kim et al., J Biol Chem 1998
-
Reactome Reaction:
IGF2
→
SHC1
(reaction)
Hernández-Sánchez et al., J Biol Chem 1995*, Tartare-Deckert et al., J Biol Chem 1995*, Giorgetti et al., Eur J Biochem 1994*, Kim et al., J Biol Chem 1998
Text-mined interactions from Literome
Vincent et al., Neurobiol Dis 2004
:
IGF-I :
IGF-IR signaling
involves phosphorylation of IRS-1 and
Shc , but not IRS-2
Maile et al., Mol Endocrinol 2006
:
In the presence of this antibody,
IGF-I stimulated
Shc phosphorylation and ERK 1/2 activation were impaired, and this was associated with an inhibition in the ability of IGF-I to stimulate an increase in migration or proliferation
Salani et al., Endocrinology 2008
:
These results demonstrate that : 1 ) Cav-1 down-regulation negatively affects IGF-IR tyrosine phosphorylation ; 2 ) this effect causes a reduced activation of insulin receptor substrate-1,
Shc , and Akt ; and 3 ) Cav-1 is
involved in
IGF-IR antiapoptotic signaling after serum deprivation
Tartare-Deckert et al., J Biol Chem 1995
:
Our findings can be summarized as follows : ( i ) the tyrosine kinase activity of the
IGF-IR is
essential for the interaction with
p52Shc and IRS-1, ( ii ) p52Shc and IRS-1 bind to the IGF-IR in the NPEY-juxtamembrane motif, ( iii ) contrary to p52Shc, IRS-1 binds also to the major autophosphorylation sites ( Tyr-1131, -1135, and -1136 ) of the IGF-IR, and ( iv ) the amino-terminal domain of p52Shc is required for its association with the IR and the IGF-IR