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CASP3 — EGFR
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Bae et al., FEBS Lett 2001
:
We have found that treatment of A431 cells with tumor necrosis factor-alpha in the presence of cycloheximide resulted in the cleavage of
epidermal growth factor receptor (EGFR) as well as the
activation of
caspase-3 ... We also investigated the effect of
caspase dependent cleavage of
EGFR upon the mediation of signals to downstream signaling molecules such as PLC-gamma1
Keese et al., Differentiation 2007
(Colorectal Neoplasms) :
We have studied
caspase-3 activation by combined DNA damage induction and
EGFR kinase inhibition in order to identify potential EGFR mediated survival signals conferring resistance to apoptosis in human colorectal tumor cells
Ge et al., Biol Reprod 2009
:
On the other hand, inhibition of
EGFR , Ca ( 2+ ) /PKC, or NFKB1 abolished the EGF stimulated increase in the expression of cyclins CCND1 and CCNE1, cyclin dependent kinase 6 (CDK6), CDK2, and BCL2, and
restored the EGF induced inhibition of BAX expression and
caspase 3/9 activity, indicating that EGFR, PKC, and NFKB1 signaling cascades were involved in EGF stimulated DNA synthesis and antiapoptosis action
Lokeshwar et al., Cancer Res 2010
(Neoplasm Invasiveness...) :
4-MU
induced caspase-8, caspase-9, and
caspase-3 activation, PARP cleavage, upregulation of Fas-L, Fas, FADD and DR4, and downregulation of bcl-2, phosphorylated bad, bcl-XL, phosphorylated Akt, phosphorylated IKB, phosphorylated ErbB2, and phosphorylated
epidermal growth factor receptor
Adam et al., Hum Reprod 2012
:
DCN, like epidermal GF, phosphorylated
EGFR significantly ( P < 0.05 ) and
reduced the activity of
caspase 3/7 in cultured GCs