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EGFR — PHKA2
Text-mined interactions from Literome
Murasawa et al., J Biol Chem 2000
(Calcium Signaling) :
Inhibition of
EGF-R did not
affect Pyk2 and JNK activation by Ang II
McCole et al., J Biol Chem 2002
:
Anti-EGFr did not
reduce CCh stimulated
Pyk-2 phosphorylation
Shi et al., J Biol Chem 2004
:
Pyk2 is a member of the focal adhesion kinase family and can be
activated by c-Src,
epidermal growth factor receptor (EGFR) , Janus kinase 1, tyrosine kinases, and G-protein coupled receptor signaling
Park et al., Cell Signal 2006
:
Using specific pharmacological inhibitors, we found that the tyrosine phosphorylation of
RAFTK/Pyk2 was intracellular Ca2+ dependent, but not
EGFR dependent , during LPA stimulation of these cells
Burdick et al., Carcinogenesis 2006
(Breast Neoplasms) :
A peak in Ca2+ concentration at 20 min was followed by increased phosphorylation of
Pyk2 at Tyr881 and
increased total tyrosine phosphorylation of the
epidermal growth factor receptor (EGFR)
Dewar et al., Mol Pharmacol 2007
(Calcium Signaling) :
Neither
EGFR kinase nor
Pyk2 inhibition prevented Src activation ; however, inhibition of Src kinase activity prevented Pyk2 activation
Lin et al., Toxicol Appl Pharmacol 2008
:
LPS stimulated Src,
PYK2 , EGFR, and Akt phosphorylation and VCAM-1 expression were
attenuated by the inhibitors of Src ( PP1 ),
EGFR ( AG1478 ), PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110
Schauwienold et al., J Biol Chem 2008
:
In vascular smooth muscle cells, both matrix-metalloproteinase dependent extracellular shedding of membrane bound
epidermal growth factor (EGF) receptor ligands and
activation of the nonreceptor tyrosine kinases
Pyk2 and Src contributed to the thrombin induced ERK1/2 phosphorylation
Block et al., J Biol Chem 2010
(Wounds and Injuries) :
Pyk2 activation
triggers epidermal growth factor receptor signaling and cell motility after wounding sheets of epithelial cells ... Disruption of Pyk2 signaling either by small interfering RNA or by expression of a dominant negative mutant led to inhibition of wound induced activation of the SFKs and the EGFR, and conversely, overexpression of wild-type
Pyk2 stimulated SFK and
EGFR kinase activities in cells