Gene interactions and pathways from curated databases and text-mining

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EGFR — FOS

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

Chen et al., J Biol Chem 2001 (Cell Transformation, Neoplastic) : Egfr gene deficiency blocked TPA induced ERK activity and AP-1 binding activity
Bancroft et al., Int J Cancer 2002 (Carcinoma, Squamous Cell...) : Recombinant EGF induced EGFR phosphorylation, activation of NF-kappaB and AP-1 reporter genes and IL-8 and VEGF expression, indicating that EGFR can mediate coactivation of both transcription factors and cytokine genes in HNSCC ... We conclude that antagonists of EGFR, PI3K and MEK signal pathways have inhibitory activity against EGFR induced NF-kappaB and AP-1 activation, IL-8 and VEGF expression and growth by HNSCC
Li et al., Oncogene 2003 : Currently, little is known about whether EGFR or its tyrosine kinase is necessary for TPA induced AP-1 activation ... Based on these results, we conclude that TPA induced AP-1 activation requires the basal level-EGFR protein, but not EGFR tyrosine kinase and EGFR autophosphorylation at tyrosine ( 1173 ), whereas both EGFR tyrosine kinase and EGFR autophosphorylation at Y ( 1173 ) play a critical role in EGF induced AP-1 activation
Das et al., J Biol Chem 2004 (Breast Neoplasms...) : Furthermore, OPN induces alpha(v)beta(3) integrin/EGFR mediated ERK1/2 phosphorylation and AP-1 activation
Ma et al., Biochem Pharmacol 2005 : Thus, EGFR plays a critical role in the interaction between ethanol and AP-1
Finch et al., Free Radic Biol Med 2006 (Carcinoma, Squamous Cell) : An EGF-R inhibitor, AG1478, blocks the higher AP-1 transactivation and cell proliferation of the low catalase 6M90 cells
Vlotides et al., Mol Endocrinol 2006 (Pituitary Neoplasms) : EGF induced EGFR and ERK1/2 phosphorylation was followed by rapid MAPK kinase/ERK kinase dependent activation of Elk-1 and c-Fos
Joo et al., Oncogene 2008 : Finally, EGFR transactivation was involved in the expression of c-Fos and c-Jun via the extracellular signal regulated kinase signaling cascade
Hsieh et al., J Cell Biochem 2008 : Moreover, S1P induced EGFR expression was inhibited by an AP-1 inhibitor curcumin and tanshinone IIA
Hsieh et al., Biochim Biophys Acta 2008 : Moreover, thrombin stimulated activation of NF-kappaB, AP-1 , and COX-2 promoter activity was blocked by the inhibitors of c-Src, PKC, EGFR , MEK1/2, AP-1 and NF-kappaB, suggesting that thrombin induces COX-2 promoter activity mediated through PKC ( delta ) /c-Src dependent EGFR transactivation, MEK-ERK1/2, AP-1, and NF-kappaB
Kajanne et al., Int J Oncol 2009 (Prostatic Neoplasms) : Here, we show that constitutive AP-1 activity in prostate cancer cells is dependent on the activities of EGF-R and PI3K ... Together, the findings show that AP-1 activity in prostate cancer cells mediates EGF-R and PI3K signalling, is essential for their proliferation, and confers protection against radiation induced cell death
Oyesanya et al., Molecular cancer 2010 (Neoplasm Invasiveness) : In ovarian cancer cells highly responsive to LPA, activation of AP-1 by LPA was suppressed by inhibition of EGFR , an effect that could be reversed by co-stimulation of another receptor tyrosine kinase c-Met with hepatocyte growth factor, indicating that LPA mediated activation of AP-1 requires activity of a RTK, not necessarily EGFR
Hwang et al., Mol Nutr Food Res 2011 (Fibrosarcoma...) : Furthermore, the EGFR inhibitor inhibited EGF induced MMP-9 expression, as well as AP-1 activity and cell migration ... Capsaicin inhibited the EGF induced invasion and migration of human fibrosarcoma cells via EGFR dependent FAK/Akt, PKC/Raf/ERK, p38 mitogen activated protein kinase ( MAPK ), and AP-1 signaling, leading to the down-regulation of MMP-9 expression
Saeki et al., Exp Dermatol 2012 : In the current study, the regulatory relationship between ErbB receptor activation and induction of AP-1 proteins in calcium dependent keratinocyte differentiation was analysed ... The predicted network showed that the ErbB receptor might regulate AP-1 protein expression via two pathways : positive regulation by c-MYC and negative regulation by signal transducer and activator of transcription 3 ( STAT3 ) pathways ... Experimental validation analysis revealed that ErbB receptor inhibition resulted in defective induction of AP-1 proteins and suppressed terminal differentiation of keratinocytes
Okimoto et al., Oncogene 1996 : Regulation of epidermal growth factor receptor by activated H-ras and V-myc oncogenes in mouse Balb/3T3 cells : possible roles of AP-1