Gene interactions and pathways from curated databases and text-mining

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CRK — EGFR

Pathways - manually collected, often from reviews:

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Nicholl et al., J Vasc Surg 2005 : Inhibition of EGFR reduced both ERK1/2 and p38 MAPK activation
Kuwahara et al., Am J Physiol Lung Cell Mol Physiol 2006 : We conclude that NE increases IL-8 transcription through p38/NF-kappaB activation via EGFR transactivation
Jiang et al., J Ocul Pharmacol Ther 2006 : EGF induced cell migration in a dose dependent manner ; EGF induced EGFR phosphorylation and downstream activation of c-Jun N-terminal protein kinase (JNK), p38 MAP kinase ( p38 ) , extracellular signal regulated kinase ( ERK1/2 ) and AKT, were inhibited by PD153035 ( EGFR inhibitor ), JNKi ( JNK inhibitor ), SB203580 ( p38 inhibitor ), U0126 ( MEK/ERK inhibitor ), and LY294002 ( PI3K/AKT inhibitor ), respectively
Harrington et al., Obesity (Silver Spring) 2007 : Our results show that EGFR homodimers mediate action of EGF at high abundance, but at low abundance, EGF promotes differentiation through EGFR/EB2R heterodimer activation of Src and p38
Taub et al., Mol Biol Cell 2007 (MAP Kinase Signaling System) : Continuous EGFR signaling from late endosomes caused sustained extracellular signal regulated kinase and p38 signaling and resulted in hyperactivation of nuclear targets, such as Elk-1
Wakasaki et al., Neoplasia (New York, N.Y.) 2010 (Carcinoma, Squamous Cell...) : Little is known, however, about a role of CIN85 in EGFR signaling as well as its relevance to tumor development and progression of HNSCC
Schroeder et al., Mol Biol Cell 2012 : In this study we show that EGFR activation leads to a pronounced src mediated tyrosine phosphorylation of CIN85 that subsequently influences EGFR ubiquitination