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INSR — PIK3CA
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Lavan et al., J Biol Chem 1992*, Hadari et al., J Biol Chem 1992*, Okamoto et al., Biochem J 1993*, Giorgetti et al., J Biol Chem 1993*
Evidence: assay
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS3 complex (INSR-INS)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Xu et al., J Biol Chem 1999*
Evidence: assay, other species
Text-mined interactions from Literome
Rogers et al., Diabetes 2008
(Adenovirus Infections, Human...) :
In turn, the activation of
PI3K by Ad-36 was
independent of
insulin receptor signaling but dependent on Ras signaling recruited by Ad-36
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
He et al., Ann Oncol 2012
(Breast Neoplasms...) :
Human epidermal growth factor receptor ( HER2 ),
insulin receptor and IGF-I receptor
involve the same
PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer
Kenzel et al., J Immunol 2012
(Inflammation...) :
We found that GBS induced, MyD88 dependent chemokine formation of PML was specifically downmodulated by insulin via
insulin receptor mediated induction of
PI3K