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EGF — PCNA
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
PCNA
→
EGF
(increases)
Olsen et al., Cell 2006*
Evidence: We have detected 6,600 phosphorylation sites on 2,244 proteins and have determined their temporal dynamics after stimulating HeLa cells with epidermal growth factor (EGF) and recorded them in the Phosida database
Text-mined interactions from Literome
Alisi et al., Cell Physiol Biochem 2003
:
EGF administered to non operated rats
increased PCNA ( proliferating cell nuclear antigen ) expression, whereas when EGF was administered to partially hepatectomized rats it was able to anticipate the increase in PCNA expression to 18h after PH and to prolong it to 34h
Heo et al., Am J Physiol Cell Physiol 2006
(MAP Kinase Signaling System) :
Finally, inhibition of EGFR tyrosine kinase, PKC, Ca2+ channels, or p44/42 MAPKs attenuated
EGF stimulated cyclin D1, cyclin E,
cyclin dependent kinase (CDK)2 , and CDK4, respectively
Vlotides et al., Mol Endocrinol 2006
(Pituitary Neoplasms) :
Phosphatidylinositol 3 kinase, protein kinase C, and MAPK, but not c-Jun N-terminal kinase and Janus activating kinase signaling regulated
EGF induced Pttg1, as well as
proliferating cell nuclear antigen mRNA expression and entry into S-phase
Xu et al., Asia Pac J Clin Nutr 2007
(Stomach Ulcer) :
Compared with the control, the UI of SBPC group was significantly lower ( p < 0.01 ) and the level of
EGF in the plasma of SBPC group
increased significantly ( p < 0.01 ), meanwhile the expression of EGFR and
PCNA around ulcer in high-dose SBPC stomach were enhanced ( p < 0.05 )
Chen et al., Mol Med Report 2010
:
PKG II activation inhibited the
EGF induced increase in
PCNA expression
Zhang et al., Toxicol Appl Pharmacol 2012
:
We found that SAHA treatment resulted in the dramatic inhibition of
EGF induced cell transformation,
cyclin D1 protein expression and induction of G0/G1 growth arrest
Bravo et al., Proc Natl Acad Sci U S A 1984
(Carcinoma) :
The
effect of
epidermal growth factor (EGF) on the synthesis of the nuclear protein
cyclin and its relationship with cell proliferation has been studied in human carcinoma A431 cells
Oberhammer et al., Carcinogenesis 1995
:
As demonstrated by immunohistochemical detection of PCNA, TGF-beta 1 prevented
induction of
PCNA by
epidermal growth factor (EGF)
Barth et al., J Cell Physiol 1995
:
Taken together, the results show that
EGF in HeLa cells very rapidly
prevents the
p34cdc2/Cyclin B complex from expressing kinase activity at the G2-M boundary, which appears to be the cause for the inhibition in G2 phase
Mark et al., Neurosci Lett 1997
:
In addition, KCl significantly reduced the
EGF induced expression of cell cycle progression factors cdk2, cdk4,
cyclin B1 and PCNA
Takuwa et al., Mol Cell Biol 1997
:
Unlike the earlier expression of Ras ( Asn17 ) at the border between G0 and G1, its delayed expression did not compromise the
EGF stimulated transient activation of extracellular signal regulated kinases or
inhibit the stimulated expression of a principal D-type
cyclin , cyclin D1, until close to the border between G1 and S
Lipson et al., J Pharmacol Exp Ther 1998
:
A synthetic EGF receptor kinase inhibitor showed selective inhibitor properties when tested for
EGF induced receptor autophosphorylation, MAPK activation, PI3K activation, entry into S phase and
cyclin E-associated kinase activity
Ikezawa et al., FASEB J 1998
:
The
cyclin E levels did not
increase in the presence of
EGF alone