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EGFR — PCNA

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PCNA — EGFR (physical association, affinity chromatography technology) Wang et al., Nat Cell Biol 2006*
• IRef Biogrid Interaction: PCNA — EGFR (direct interaction, enzymatic study) Wang et al., Nat Cell Biol 2006*

Text-mined interactions from Literome

Psyrri et al., Med Oncol 2006 (Carcinoma, Squamous Cell...) : Cyclin dependent kinases, the tumor suppressor p53 gene, and epidermal growth factor receptor are some of the molecular targets of such therapies in patients with SCCHN
Rougier et al., Semin Oncol 2007 (Carcinoma, Hepatocellular...) : Possible future therapeutic strategies include epidermal growth factor receptor inhibitors, antivascular endothelial growth factor therapies, cyclin D inhibitors , and HMG-CoA reductase inhibitors
Yang et al., Biochem J 2008 (Breast Neoplasms) : Inhibition of EGFR , PI3K ( phosphoinositide 3-kinase ; kinases required for Rac activation by HRG ) or MEK [ MAPK ( mitogen activated protein kinase ) /ERK ( extracellular-signal regulated kinase ) kinase ] also blocked the up-regulation of cyclin D1 and p21(Cip1) by HRG
Lee et al., American journal of physiology. Renal physiology 2008 : Consequently, the inhibition of Ca ( 2+ ), PKC, EGFR , p44/42 MAPKs, or NF-kappaB blocked the BSA induced increases in cyclin D1, cyclin dependent kinase (CDK)4 , cyclin E, or CDK2 and restored the BSA induced inhibition of p21 ( WAF/Cip1 ) and p27 ( Kip1 ) expression