Gene interactions and pathways from curated databases and text-mining

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EPHB2 — GAB2

Text-mined interactions from Literome

Dorsey et al., Blood 2002 (Leukemia, Myeloid) : Analysis of these cell lines indicated that induction of Gab2WT expression, but not Gab2Tyr604Phe expression, led to Erk activation, growth arrest, cell spreading, and enlargement ; expression of megakaryocyte/platelet lineage-specific integrins alphaIIb/beta3 ( CD41/CD61 ) ; and upregulation of RNA for megakaryocyte/platelet proteins
Yu et al., Blood 2002 : Biochemical analyses revealed that enforced expression of Gab2 mutant molecules dramatically reduced beta ( 1 ) -integrin ligation triggered PI3 kinase activation, whereas Erk kinase activation remained unaltered
Koncz et al., Immunol Lett 2002 : Since ERK is regulated by the phosphorylated Gab1/2 , these data demonstrate that BCR triggered phosphorylation and signal amplification of Gab1/2 is a critical step in a life or death decision of B cells
Arnaud et al., Biochem J 2004 (Leukemia, Prolymphocytic, T-Cell) : Expression of the Gab2 Tyr-614 -- > Phe ( Y614F ) mutant, defective in SHP-2 association, prevents ERK ( extracellular-signal regulated kinase ) activation and expression of a luciferase reporter plasmid driven by the c-fos SRE ( serum response element ), indicating that interaction of SHP-2 with Gab2 is required for ERK activation in response to IL-2
Arnaud et al., J Immunol 2004 (MAP Kinase Signaling System) : This migration shift was strongly diminished by treating cells with the MEK inhibitor U0126, indicating a possible role for ERK in Gab2 phosphorylation ... We report that pretreatment of Kit 225 cells with U0126 increased Gab2/SHP-2 association and tyrosine phosphorylation of SHP-2 in response to IL-2, suggesting that ERK phosphorylation of serine 623 regulates the interaction between Gab2 and SHP-2, and consequently the activity of SHP-2
Mao et al., J Cell Biol 2005 : Gab2 suppression reduces bFGF dependent activation of AKT but not ERK , and constitutively active AKT, but not constitutively active MEK1, reverses the hypersensitization
Simoncic et al., Mol Cell Biol 2006 : Tcptp-/- macrophages also have increased tyrosine phosphorylation and recruitment of a Grb2/Gab2/Shp2 complex to the CSF-1R and enhanced activation of Erk after CSF-1 stimulation, which are important molecular events in CSF-1 induced differentiation