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EGF — IRS2
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
IRS2
→
EGF
(increases)
Olsen et al., Cell 2006*
Evidence: We have detected 6,600 phosphorylation sites on 2,244 proteins and have determined their temporal dynamics after stimulating HeLa cells with epidermal growth factor (EGF) and recorded them in the Phosida database
Text-mined interactions from Literome
Lingohr et al., Diabetes 2002
(MAP Kinase Signaling System) :
Neither IRS-1 nor
IRS-2 overexpression
induced a beta-cell proliferative response to
TGF-alpha/EGF
Gogg et al., J Biol Chem 2002
(Insulin Resistance) :
EGF increased the tyrosine phosphorylation of several proteins ( the EGF receptor, insulin receptor substrate (IRS)-1,
IRS-2 , and Grb2 associated binder 1 ), whereas Shc and Gab2 were only weakly and inconsistently phosphorylated ... Both insulin and
EGF increase the tyrosine phosphorylation and activation of IRS-1 and
IRS-2 , whereas EGF is also capable of activating additional PI 3-kinase pools and, thus, can augment the downstream signaling of insulin in insulin-resistant states like Type 2 diabetes
Cui et al., Cancer Res 2006
(Breast Neoplasms) :
Although both extracellular signal regulated kinase and c-Jun NH ( 2 ) -terminal kinase ( JNK ) signaling pathways were involved in the EGF up-regulation of IRS-1, the
IRS-2 induction by
EGF was specifically mediated by JNK signaling ... Consistent with this,
EGF increased
IRS-2 promoter activity, which was associated with recruitment of activator protein-1 (AP-1) transcription factors and was inhibited by blocking AP-1 activity ... Finally, repressing the induction of IRS-2 levels abolished the EGF enhancement of cell motility, suggesting that increased
IRS-2 is
essential for the
EGF regulation of breast cancer cell migration