Gene interactions and pathways from curated databases and text-mining

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EGFR — HSP90AA1

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

Xu et al., Br J Cancer 2007 (Carcinoma, Non-Small-Cell Lung...) : The mature epidermal growth factor receptor (EGFR) neither associates with nor requires the molecular chaperone heat-shock protein 90 (Hsp90)
Ahsan et al., Neoplasia (New York, N.Y.) 2012 (Head and Neck Neoplasms...) : Wild-type EGFR is stabilized by direct interaction with HSP90 in cancer cells and tumors ... Further, the HSP90 inhibitors geldanamycin ( GA ) and AT13387 cause a decrease in WT-EGFR in cultured head and neck cancer cells
Sawai et al., Cancer Res 2008 (Carcinoma, Non-Small-Cell Lung...) : Hsp90 inhibitors, such as 17-allylamino-17-demethoxygeldanamycin ( 17-AAG ), induce the degradation of EGFR and other Hsp90 interacting proteins and may thus have utility in tumors dependent upon sensitive Hsp90 clients
El Hamidieh et al., PloS one 2012 (Breast Neoplasms...) : Finally, we show that functional inhibition of surface HSP90 using mAb 4C5, a cell impermeable monoclonal antibody against this protein, leads not only to disruption of the Cdc37/HSP90 complex but also to inhibition of the Cdc37/ErbB receptors complexes
Adachi et al., Oncol Rep 2010 (Pancreatic Neoplasms) : These results strongly suggest that EGFR phosphorylation at Ser1046/7 via activation of p38 MAPK induced by HSP90 inhibitors plays a pivotal role in EGFR desensitization in human pancreatic cancer cells