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PIK3R1 — POT1

Text-mined interactions from Literome

York et al., Mol Cell Biol 2000 : We show here that Rap1 activation requires both TrkA internalization and PI3-K , whereas Ras activation requires neither TrkA internalization nor PI3-K
Woulfe et al., J Biol Chem 2002 : Finally, using human platelets treated with selective inhibitors of phosphatidylinositol 3-kinase (PI3K) and mouse platelets selectively lacking the G ( beta ) ( gamma ) -activated form of his enzyme ( PI3Kgamma ), we show that G ( i ) -mediated Rap1 activation is PI3K dependent
Romano et al., Endocrinology 2006 : Under the same conditions, PI3K and Akt inhibition also both increased Raf-1 kinase activity and the levels of GTP bound ( active form ) monomeric G protein Rap1 , which suggests that a down-regulation of the ERK-1/2 cascade is induced by the PI3K/Akt signaling pathway in unstimulated cells
Li et al., J Biol Chem 2008 : Inhibition of PI3K or mTOR reduced the level of Rap1B , which acts downstream of Rheb and mTOR
Schmid et al., PloS one 2013 (Inflammation...) : Genetic depletion of PLC?, CalDAG-GEFI or II, Rap1a , or the Rap1 effector RIAM was sufficient to prevent integrin a4 activation by chemoattractants or activated PI3K? ( p110?CAAX ), while activated Rap ( RapV12 ) promoted constitutive integrin activation and cell adhesion that could only be blocked by inhibition of RIAM or integrin a4ß1