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EPHB2 — PTK2
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Yu et al., Am J Physiol Gastrointest Liver Physiol 2000
:
Caco-2 motility was inhibited by transfection of
FRNK ( the COOH-terminal region of FAK ) and PD-98059, a mitogen activated protein
kinase-ERK kinase
inhibitor , but not by SB-203580, a p38 inhibitor, suggesting that FAK and ERK modulate Caco-2 migration
Frank et al., Endocrinology 2000
:
In this regard, H2O2 and a membrane permeable thiol oxidizing agent, diamide, stimulated protein tyrosine phosphorylation of p120 and p70, and
ERK activation in VSMCs. H2O2 also
enhanced PTK activity
Govindarajan et al., Circ Res 2000
:
Similarly,
FRNK overexpression
blocked Ang II-induced FAK phosphorylation and
ERK1/2 activation, but not p70 ( S6K ) phosphorylation, and markedly inhibited protein synthesis
Akhand et al., Free Radic Biol Med 2001
(MAP Kinase Signaling System) :
These results demonstrated that GO and MGO triggered two distinct signal cascades, one for
PTK dependent control of
ERK and another for PTK independent redox linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals
Hauck et al., Cancer Res 2001
(Adenocarcinoma...) :
Adenoviral mediated infection and expression of
FRNK promoted FAK dephosphorylation at Tyr-397,
resulted in reduced EGF stimulated JNK as well as
extracellular regulated kinase 2 (ERK2) kinase activation, inhibited matrix metalloproteinase-9 (MMP-9) secretion, and potently blocked both random and EGF stimulated A549 cell motility
Duchemin et al., J Neurochem 2002
:
Pertussis toxin, as well as Src
protein tyrosine kinase and protein kinase C inhibitors, did not
prevent the GM1 induced activation of
Erk2 , apparently excluding the participation of Gi and Gq/11 protein coupled receptors
Heidkamp et al., Circ Res 2002
:
In contrast,
GFP-FRNK overexpression did not
prevent ET-induced
ERK , JNK, or p70S6K phosphorylation
Hauck et al., EMBO J 2002
(Lung Neoplasms) :
FRNK expression disrupted the formation of a v-Src-FAK signaling complex, inhibited p130Cas tyrosine phosphorylation, and
attenuated v-Src stimulated
ERK and JNK kinase activation
Yu et al., J Biol Chem 2003
:
IL-6 increased phosphorylation of STAT3 ( at Tyr ( 705 ) ) and ERK1/2 ( at Tyr ( 204 ) ) within 5 min that peaked at 15-30 min and returned to basal levels at 2 h. Phosphorylation of STAT3 was blocked by genistein, a
protein tyrosine kinase inhibitor, and AG490, a JAK2 inhibitor, but not PD98059, an
ERK1/2 kinase
inhibitor
Bian et al., Exp Eye Res 2003
(Translocation, Genetic) :
These results suggest that activation of DEX-sensitive, CSA-resistant
MEK/ERK and p38 pathways, and
activation of NF-kappaB, PKC, and
PTK are essential for IL-8 and MCP-1 expression by hRPE cells
Ogasawara et al., Int J Hematol 2003
(Leukemia, B-Cell...) :
We found that Lyn
protein tyrosine kinase was constitutively phosphorylated on tyrosine, and that
ERK and p38 MAPK were constitutively
active in all cases of the B-cell tumor
Kobayashi et al., Vet Immunol Immunopathol 2005
:
Moreover, the ConA induced IFN-gamma mRNA expression was partly prevented by genistein, a global
PTK inhibitor, and PD-98059, an
ERK inhibitor , respectively
Sawhney et al., J Biol Chem 2006
(Colonic Neoplasms) :
Ectopic expression of the FAK C-terminal domain
FRNK attenuated FAK and
ERK phosphorylation and micromotion
Hisaoka et al., J Pharmacol Exp Ther 2007
:
Taken together, these findings indicate that
ERK activation through
PTK regulates antidepressant induced GDNF production and that the GDNF production in glial cells may be a novel action of the antidepressant, which is independent of monoamine
Lal et al., J Mol Cell Cardiol 2007
:
In the presence of ATB,
FRNK overexpression significantly
increased basal phosphorylation of
ERK ( 40.2+/-8.6 % P < 0.05 ), p38 ( 39.5+/-11.7 %, P < 0.05 ), JNK ( 86+/-29.4 %, P < 0.05 ) and stretch induced p38 ( 48.1+/-8.7 %, P < 0.05 ) and JNK ( 85.0+/-19.4 %, P < 0.05 ) phosphorylation ... However, in the absence of ATB,
FRNK overexpression significantly reduced basal and stretch
induced phosphorylation of only
ERK
Park et al., Mol Cells 2008
(Neoplasms) :
FRNK , an inhibitory fragment of FAK,
inhibited ERK and decreased motility
Ding et al., J Biol Chem 2008
(Disease Models, Animal...) :
FRNK overexpression
blocks TGF-beta1 induced
ERK or p38 MAPK activation in the presence, and surprisingly, in the absence of FAK
Chung et al., Arch Pharm Res 2008
:
Whereas the
PTK inhibitor, genistein, partially
inhibited ERK1/2 activation, the EGFR tyrosine kinase inhibitor, tyrphostin 51, had no effect
Liu et al., Lab Invest 2009
(Liver Cirrhosis) :
We provide evidence that
PTK787/ZK222584 ( PTK/ZK ) , a potent tyrosine kinase inhibitor that blocks vascular endothelial growth factor receptor ( VEGFR ), significantly
inhibits PDGF receptor expression, as well as PDGF simulated HSC proliferation, migration and phosphorylation of
ERK1/2 , Akt and p70S6 kinase
Sánchez et al., Chem Biol Interact 2009
:
On the other hand, the
PTK inhibitors
caused disparate effects on
ERK phosphorylation, and co-treatment with the MEK/ERK inhibitor PD98059 enhanced the pro-apoptotic capacity of the PTK inhibitors
Agarwal et al., J Biol Chem 2010
:
We also show that functionally active Src
PTK is
essential for activation of
ERK1/2 upon pneumococcal infections
Schlaepfer et al., J Biol Chem 1997
:
FN-stimulated c-Src
PTK activity was
enhanced by wild type FAK expression, whereas FN-stimulated activation of
ERK2 was blocked by expression of the c-Src binding site Phe-397 mutant of FAK
Sieg et al., EMBO J 1998
:
Significantly, repression of endogenous Src-family
PTK activity by p50 ( csk ) overexpression
inhibited FN-stimulated cell spreading, Pyk2 tyrosine phosphorylation, Grb2 binding to Shc, and
ERK2 activation in the FAK- but not in FAK+ cells