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AKT1 — GAB2

Pathways - manually collected, often from reviews:

• NCI Pathway Database Fc-epsilon receptor I signaling in mast cells: GAB2/PI3K/SHP2 complex (GAB2-PTPN11-PIK3CA-PIK3R1) → AKT1 (AKT1) (modification, activates)
• NCI Pathway Database IL6-mediated signaling events: GRB2/SOS1/GAB family/SHP2/PI3K complex (GRB2-SOS1-GAB1_GAB2-PTPN11-PIK3CA-PIK3R1) → AKT1 (AKT1) (modification, activates) Jee et al., J Invest Dermatol 2002
  Evidence: mutant phenotype

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: AKT1 — GAB2 (physical association, affinity chromatography technology) Lynch et al., EMBO J 2002*
• IRef Biogrid Interaction: AKT1 — GAB2 (direct interaction, enzymatic study) Lynch et al., EMBO J 2002*
• IRef Hprd Interaction: AKT1 — GAB2 (in vitro) Lynch et al., EMBO J 2002*
• IRef Hprd Interaction: AKT1 — GAB2 (in vivo) Lynch et al., EMBO J 2002*
• IRef Innatedb Interaction: AKT1 — GAB2 (unknown, -) Lynch et al., EMBO J 2002*
• IRef Ophid Interaction: AKT1 — GAB2 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Lynch et al., EMBO J 2002 : This represents phosphorylation by the serine/threonine kinase protein kinase B (PKB), since PKB constitutively associates with Gab2, phosphorylates Gab2 on a consensus phosphorylation site, Ser159, in vitro and inhibits Gab2 tyrosine phosphorylation
Million et al., Mol Cell Biol 2004 (Cell Transformation, Neoplastic...) : A Tel-Abl point mutant ( Y314F ) and a splice variant without TEL exon 5 sequences ( Deltae5 ) lacked Grb2 interaction and exhibited decreased binding and phosphorylation of the scaffolding protein Gab2 and impaired activation of phosphatidylinositol 3-kinase, Akt , and extracellular signal regulated kinase/mitogen activated protein kinase in hematopoietic cells
Nyga et al., Biochem J 2005 : Taken together, our results indicate that Gab2 is required for caSTAT5 induced cell proliferation by regulating both the PI3K/Akt and the Ras/MAPK pathways
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 ... Thus, Gab2 mediated AKT activation is required for bFGF 's protection
Abramson et al., EMBO J 2006 : Specifically, MAFA suppresses the PLC-gamma2- [ Ca2+ ] i, Raf-1-Erk1/2, and PKC-p38 coupling pathways, while the Fyn-Gab2 mediated activation of PKB and Jnk is essentially unaffected
Maus et al., Cell Signal 2009 : It has been shown in several model systems that Gab/Dos family members may regulate both the anti-apoptotic PI3-K/Akt and the mitogenic Ras/MAPK pathways, still their role in B-cells have not been investigated in detail
Huang et al., Cell Mol Immunol 2008 (Calcium Signaling) : Treatment with Gab2 siRNA significantly decreased Gab2 expression, inhibited the FcepsilonRI mediated mast cell release of beta-hexosaminidase and histamine, reduced the production of IL-4 and TNF-alpha and inhibited the phosphorylation of Akt , PKCdelta and p38 mitogen activated protein kinase ( MAPK )
Hunzicker-Dunn et al., Proc Natl Acad Sci U S A 2012 : Overexpression of GAB2 enhances FSH stimulated AKT phosphorylation