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PIK3CA — TERF1
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
Gilio et al., J Biol Chem 2009
(Thrombosis) :
Furthermore,
PI3Kalpha/beta , but not PI3Kgamma,
contributed to GPVI induced
Rap1b activation and, surprisingly, also to Rap1b independent platelet activation via GPVI
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