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Epiregulin: roles in normal physiology and cancer.
Riese, David J; Cullum, Richard L.
Afiliação
  • Riese DJ; Department of Drug Discovery and Development, Harrison School of Pharmacy, 2316 Walker Building, Auburn University, Auburn, AL 36849, USA. Electronic address: driese@auburn.edu.
  • Cullum RL; Department of Chemical Engineering, Samuel Ginn College of Engineering, Auburn, AL 36849, USA. Electronic address: rlc0029@auburn.edu.
Semin Cell Dev Biol ; 28: 49-56, 2014 Apr.
Article em En | MEDLINE | ID: mdl-24631357
ABSTRACT
Epiregulin is a 46-amino acid protein that belongs to the epidermal growth factor (EGF) family of peptide hormones. Epiregulin binds to the EGF receptor (EGFR/ErbB1) and ErbB4 (HER4) and can stimulate signaling of ErbB2 (HER2/Neu) and ErbB3 (HER3) through ligand-induced heterodimerization with a cognate receptor. Epiregulin possesses a range of functions in both normal physiologic states as well as in pathologic conditions. Epiregulin contributes to inflammation, wound healing, tissue repair, and oocyte maturation by regulating angiogenesis and vascular remodeling and by stimulating cell proliferation. Deregulated epiregulin activity appears to contribute to the progression of a number of different malignancies, including cancers of the bladder, stomach, colon, breast, lung, head and neck, and liver. Therefore, epiregulin and the elements of the EGF/ErbB signaling network that lie downstream of epiregulin appear to be good targets for therapeutic intervention.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Fator de Crescimento Epidérmico / Receptores ErbB / Epirregulina / Neoplasias Limite: Animals / Humans Idioma: En Revista: Semin Cell Dev Biol Assunto da revista: EMBRIOLOGIA Ano de publicação: 2014 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Fator de Crescimento Epidérmico / Receptores ErbB / Epirregulina / Neoplasias Limite: Animals / Humans Idioma: En Revista: Semin Cell Dev Biol Assunto da revista: EMBRIOLOGIA Ano de publicação: 2014 Tipo de documento: Article