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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