Gene interactions and pathways from curated databases and text-mining

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PI3 — TYR

Text-mined interactions from Literome

Maraldi et al., Adv Enzyme Regul 1999 (Osteosarcoma) : The results of this study indicate that in Saos-2 cells PI 3-kinase is recruited and activated by IL-1 receptor I (IL-1RI) through binding of the SH2 domains to the consensus sequence on the C-terminal tail of the receptor, and that Tyr-479 is essential for PI 3-kinase activation
Hers et al., Biochem J 2002 : Inhibition of PI 3-kinase enhanced the insulin stimulated phosphorylation of IRS-1 on (i) Tyr ( 612 ) and Tyr ( 941 ) ( p85 binding sites ), concomitant with an increased association of the p85 subunit of PI 3-kinase ; ( ii ) Tyr ( 896 ) ( a Grb2 binding site ) ; and ( iii ) Tyr ( 1229 ) ( an SHP-2 binding site ), although little or no binding of SHP-2 to IRS-1 was detectable under any conditions ... Furthermore, insulin induced insulin receptor tyrosine phosphorylation, phosphorylation of Tyr ( 1158 ) and insulin receptor tyrosine kinase activity were all reduced by inhibition of PI 3-kinase at later time points ( > or=20 min )
Reedijk et al., EMBO J 1992 : Tyr721 was also critical for the association of activated CSF-1R with PI 3'-kinase in mammalian cells
Momose et al., J Immunol 2003 : The class Ia phosphoinositide (PI) 3-kinase consisting of p110 catalytic and p85 regulatory subunits is activated by Tyr kinase linked membrane receptors such as FcgammaRII through the association of p85 with the phosphorylated receptors or adaptors
Damen et al., J Biol Chem 1995 : Moreover, both in vitro competition studies, involving phosphorylated peptides corresponding to the amino acid sequences flanking the eight tyrosines within the intracellular domain of the EpR, and in vivo studies with mutant EpRs bearing tyrosine to phenylalanine substitutions, indicate that phosphorylation of Tyr503 within the EpR is essential for the binding of PI 3-kinase
de Aós et al., J Biol Chem 1997 : Mutagenesis studies in COS-7 cells, transiently transfected with CD8-epsilon, p85alpha, and Fyn cDNAs in various combinations, show that both Tyr170 and Tyr181 within the CD3-epsilon-ITAM are required for efficient binding of p85alpha PI 3-kinase