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IGF2 — PIK3R1
Text-mined interactions from Literome
Hallmann et al., J Biol Chem 2003
(MAP Kinase Signaling System) :
Although,
IGF-1 stimulated
PI3K activity associated with insulin receptor substrates was unaltered in all cell lines, p85alpha-null ES cells showed diminished protein kinase B activation despite increased PI3K activity associated with the p85beta subunit
Aikin et al., Endocrinology 2004
:
In addition,
IGF-I suppressed cytokine mediated JNK activation in a
PI3K dependent manner
Ray et al., Int J Oncol 2007
(Breast Neoplasms...) :
MCF-7 cells expressed higher levels of Ob-Rb, Jak2,
PI3K , Stat3 and p-Stat3 in a dose dependent manner to 50 ng/ml at 24 h ; and
IGF-IRalpha increased at 24 h. Cyclin D1 and Cox-2 levels increased with leptin treatment
Brady et al., Growth Horm IGF Res 2008
:
IGF-I and -II caused significant increases in
PI3-K , but not MAPK, activity
Codina et al., Gen Comp Endocrinol 2008
:
Metabolic and mitogenic effects of IGF-II in rainbow trout ( Oncorhynchus mykiss ) myocytes in culture and the
role of
IGF-II in the
PI3K/Akt and MAPK signalling pathways
Hamamura et al., Cell Biol Int 2008
:
LY294002 did not suppress upregulation of TGFbeta mRNA induced by IGF2, so
IGF2 activates
PI3K and TGFbeta pathways
Koutros et al., Cancer Res 2010
(Genetic Predisposition to Disease...) :
In conclusion, we observed a significant association between PIK3C2B and prostate cancer risk, especially for familial, early-onset disease, which may be attributable to
IGF dependent
PI3K signaling
Fox et al., Cancer Res 2011
(Adenocarcinoma...) :
Inhibition of InsR and
IGF-IR with the dual tyrosine kinase inhibitor OSI-906 prevented the emergence of hormone independent cells and tumors in vivo,
inhibited parental and LTED cell growth and
PI3K/AKT signaling, and suppressed growth of established MCF-7 xenografts in ovariectomized mice, whereas treatment with the neutralizing IGF-IR monoclonal antibody MAB391 was ineffective
Appleman et al., Mol Cancer Res 2012
:
Interestingly, we find that activation of
PI3K/AKT signaling occurs downstream of MAP-ERK kinase ( MEK ), and is
dependent on the autocrine activation of the insulin-like growth factor (IGF) receptor ( IGF1R ) by
IGF2