ERBB2, present at low levels in normal cells, is overexpressed in cancer cells with ERBB2 gene amplification, leading to growth factor-independent activation of ERBB2 signaling through formation of ERBB2 homodimers (Pickl and Ries 2009, Maadi et al. 2018). It is assumed that during homodimerization, similar to normal heterodimerization with ligand-activated ERBB family members, chaperone proteins HSP90 and CDC37, as well as ERBB2IP, dissociate from ERBB2 (Borg et al. 2000, Xu et al. 2001, Citri et al. 2004).
Pickl, M, Ries, CH
Nami, B, Wang, Z, Maadi, H, Li, G, Tong, J
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