Gene interactions and pathways from curated databases and text-mining

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IGF1 — MAP2K1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Dunn et al., Cancer Res 2001 (Breast Neoplasms...) : In summary, we conclude that IGF-I requires both phosphatidylinositol 3-kinase and mitogen activated protein kinase kinase dependent pathways to optimally induce uPA expression
Mehrhof et al., Circulation 2001 : IGF-I also induced phosphorylation of cAMP response element binding protein ( CREB ) in a PI3K- and MEK1 dependent manner
Shibata et al., Life Sci 2009 : IGF-1 induced phosphorylation of extracellular related kinase (ERK)1/2, MAP or ERK kinase (MEK)1/2 , and Akt, expression of cyclin D1, and MC proliferation in cultured human MCs ... Fluvastatin or PD98059, an MEK1 inhibitor, completely abolished IGF-1 induced MEK1/2 and ERK1/2 phosphorylation and MC proliferation, whereas inhibition of Akt had no effect on MC proliferation ... Mevalonic acid prevented fluvastatin inhibition of IGF-1 induced MEK1/2 and ERK1/2 phosphorylation, cyclin D1 expression, and MC proliferation
Jiang et al., Am J Physiol Endocrinol Metab 2011 (MAP Kinase Signaling System) : In carp pituitary cells, IGF-I and -II could induce rapid phosphorylation of IGF-I receptor, MEK1/2 , ERK1/2, MKK3/6, and p38 MAPK ; and SLa and SLß secretion, protein production, and mRNA expression caused by IGF-I and -II stimulation were negated by inactivating MEK1/2 and p38 MAPK