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EPHB2 — SOS1
Text-mined interactions from Literome
Takeuchi et al., Am J Physiol 1999
:
To examine the functional
role of
Sos in
ERK2 activation, we transfected parietal cells with the HA-ERK2 vector together with a dominantly expressed mutant ( inactive ) sos gene ... Dominant negative
Sos did not
affect carbachol stimulation of
HA-ERK2 but inhibited the stimulatory effect of EGF by 60 %
Sajan et al., J Biol Chem 1999
:
In addition to requirements for PI3K, PDK-1, and PKC-zeta, we found that a tyrosine kinase ( presumably the insulin receptor ), the SH2 domain of GRB2,
SOS , RAS, RAF, and MEK1 were
required for insulin effects on
ERK in the rat adipocyte
Kimura et al., Cancer Res 1999
(Ovarian Neoplasms) :
Activation of
ERK by GnRHa occurred within 5 min, with the maximum occurring at 3 h and sustained until 24 h. GnRHa also activated ERK kinase ( mitogen activated protein/ERK kinase ) and
resulted in an increase in phosphorylation of
son of sevenless ( Sos ) , and Shc
Caverzasio et al., J Bone Miner Res 2000
:
In contrast to their implication in epidermal growth factor (EGF) receptor tyrosine kinase signaling, the adaptor protein Shc, the
Grb2/Sos complex, and the small G protein Ras were not
involved in the activation of
Erk induced by either LPA or PGF2alpha in MC3T3-E1 cells, suggesting that activation of Erk by Gi and Gq protein coupled receptors is Ras independent in these cells
Nakamura et al., Oncogene 2002
(MAP Kinase Signaling System) :
Here we determined the efficacy of Shc and N-Shc toward Erk activation in NGF treated PC12 cells, and found that N-Shc transduced
Grb2/Sos/Ras dependent
Erk activation less efficiently than Shc
Correa-Meyer et al., Am J Physiol Lung Cell Mol Physiol 2002
(MAP Kinase Signaling System) :
The inhibition of
Grb2-SOS interaction with an SH3 binding sequence peptide, Ras with a farnesyl transferase inhibitor, and Raf-1 with forskolin did not
affect the stretch induced
ERK1/2 phosphorylation
Yamasaki et al., Oncogene 2003
(Cell Transformation, Neoplastic) :
EGF dependent GTP/GDP exchange activity for Ras was suppressed in the Gab1-/- cells and expression of a constitutively active
Sos restored
ERK activation in these cells, indicating that Gab1 functions upstream of Ras
Warnecke et al., EMBO Rep 2012
:
We found that T-cell antigen receptor ( TCR ) -mediated
Erk activation
requires RasGRP1, but not
Grb2/Sos
Peng et al., PloS one 2012
:
LPS induces ubiquitin mediated degradation of DOK3 leading to
SOS1 degradation and
inhibition of
ERK activation
Samoylenko et al., Carcinogenesis 2012
(Adenocarcinoma...) :
Thereby, Ruk ( l )
/CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src, Akt and
ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility
Foschi et al., EMBO J 1997
:
We demonstrate that ET-1 signaling elicits a negative feedback mechanism, modulating p21ras activity through
ERK dependent
Sos1 phosphorylation, findings which were confirmed using an adenovirus MEK construct