glycosylation; human epidermal growth factor receptor 2 (ErbB2)

Autores e Afiliações:

Henrique O. Duarte^1,2,3, Meritxell Balmaña^1,2, Stefan Mereiter^1,2, Hugo Osório^1,2,4, Joana Gomes^1,2 and Celso A. Reis^1,2,3,4

¹Institute for Research and Innovation in Health (i3S), University of Porto, 4200-135 Porto, Portugal

²Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), 4200-135 Porto, Portugal

Cell surface receptor tyrosine kinases (RTKs) play a central role in the initiation, promotion and progression of multiple human cancers, by triggering the aberrant activation of downstream signaling pathways implicated in malignant cell phenotype and behavior. In particular, overexpression of the human epidermal growth factor 2 (ErbB2) RTK constitutes a well-established molecular driver of carcinogenesis. RTK maturation is tightly regulated by protein N-linked glycosylation.