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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to CRK

CRK — EGF

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: CRK → 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

Take et al., Biochem Biophys Res Commun 2000 : Our results suggest that CIN85 may play a specific role in the EGF receptor mediated signaling cascade via its interaction with c-Cbl
Jope et al., Arch Biochem Biophys 2000 (MAP Kinase Signaling System) : Activation of p38 by peroxynitrite was independent of the EGF receptor, required activation of calcium/calmodulin dependent kinase II and src family tyrosine kinases, and was modulated by nerve growth factor (NGF) in a time dependent manner
Rhee et al., Mol Cells 2000 : Major effects of EGF/K252a , found also in the NGF treated cells, are the sustained mobility shift of paxillin in SDS-PAGE and the promoted association of Crk-II with paxillin
Liu et al., Br J Cancer 2001 (Uterine Cervical Neoplasms) : EGF did not stimulate PI-3K/Akt, MEK/MAPK, or p38 MAPK activity in SiHa cells but did transiently activate the c-Jun NH2-terminal kinase (JNK)
Kowanetz et al., J Biol Chem 2003 : Identification of a novel proline-arginine motif involved in CIN85 dependent clustering of Cbl and down-regulation of epidermal growth factor receptors
Mata et al., Thorax 2005 : Roflumilast also inhibited the EGF induced expression of phosphotyrosine proteins, EGF receptor, and phospho-p38- and p44/42-MAPK measured by Western blot analysis in A549 cells
Johnstone et al., Placenta 2005 : We here show that the c-Jun NH2 terminal kinase (JNK) and the mitogen activated kinase ( MAPK ) p38 are also activated by EGF as seen by increases in JNK and p38 phosphorylation
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 : Both low and high EGF activated ERK and p38 in preadipocytes ... Selective inhibition of the EGF receptor (EGFR) with AG1478 blocked ERK and p38 activation at both concentrations ; however, selective inhibition of the ErbB2 receptor (EB2R) with AG825 or small interfering RNA ( siRNA ) blocked low but not high EGF activation of ERK and p38
Brusevold et al., J Oral Pathol Med 2012 (Carcinoma, Squamous Cell...) : In the E10 cell line, EGF and HGF induced phosphorylation of EGF receptor (EGFR) and Met, respectively, phosphorylation of ERK1/2, p38 and Akt, and dose dependent activation of cell migration
Inoue et al., J Oral Sci 2012 (Carcinoma, Squamous Cell...) : Furthermore, it has been reported that Src directly associates with the epidermal growth factor receptor (EGFR) in OSCC cells upon stimulation with EGF and phosphorylates Crk associated substrate (Cas) , podoplanin acting downstream of Src and Cas to promote cell migration
Iwayama et al., Mol Cell Biochem 2013 : Effect of ceramide on expression of mitochondrial Bax and phosphorylated ( p ) -ERK, p38MAPK and JNK, that of MAPKs inhibition, and of EGF in the presence or absence of MAPKs inhibition on ceramide induced apoptosis were examined in HK-2 cells
Fajardo et al., Mol Cell Biol 1993 : Furthermore, the in vivo experiments suggest that binding of Crk proteins to the stimulated EGF receptor results in Crk phosphorylation and subsequent loss of binding affinity
Ribon et al., J Biol Chem 1996 (Adrenal Gland Neoplasms...) : To further explore the role of Crk in NGF induced PC-12 cell differentiation, we found that both NGF and epidermal growth factor stimulate the tyrosine phosphorylation of endogenous Crk II
Ishiki et al., Endocrinology 1997 : We examined the potential role of Crk-II in insulin and epidermal growth factor (EGF) signaling in Rat-1 fibroblasts overexpressing insulin receptors ... Insulin- and EGF induced association of Crk-II with these molecules was assessed by immunoblotting of anti-Crk-II precipitates in Rat-1 fibroblasts overexpressing insulin receptors ... Basal tyrosine phosphorylation of c-abl and its constitutive association with Crk-II were not further increased by insulin or EGF ... Interestingly, EGF , but not insulin, stimulated tyrosine phosphorylation of c-cbl and its association with Crk-II