Non-canonical Activation of Receptor Tyrosine Kinases in Cancer Progression

DOI Web Site Web Site PubMed 25 References Open Access
  • Sakurai Hiroaki
    Department of Cancer Cell Biology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama

Bibliographic Information

Other Title
  • チロシンキナーゼ型受容体の非定型的活性化：がん病態制御の次なる標的
  • Symposium Review チロシンキナーゼ型受容体の非定型的活性化:がん病態制御の次なる標的
  • Symposium Review チロシンキナーゼガタ ジュヨウタイ ノ ヒテイケイテキ カッセイカ:ガン ビョウタイ セイギョ ノ ツギ ナル ヒョウテキ

Search this article

Abstract

 Receptor tyrosine kinases (RTKs) are known to be key regulators of cancer cell proliferation, migration, invasion and metastatic spread. Ligand-binding to the extracellular domain triggers canonical activation of the intracellular tyrosine kinase domain. In contrast, it has become evident that RTKs are also regulated by non-canonical tyrosine kinase-independent mechanisms via phosphorylation of their serine/threonine residues. In this review, I mainly introduce our recent findings on the non-canonical regulation of epidermal growth factor receptor (EGFR), ErbB2 and erythropoietin-producing hepatocellular receptor A2 (EphA2), and discuss the roles of non-canonical activation of RTKs in cancer progression and resistance to targeted cancer agents. Further characterization of non-canonical regulation will contribute to the development of new target cancer therapies.<br>

Journal

  • YAKUGAKU ZASSHI

    YAKUGAKU ZASSHI 137 (2), 141-144, 2017-02-01

    The Pharmaceutical Society of Japan

References(25)*help

See more

Related Projects

See more

Keywords

Details 詳細情報について

Report a problem

Back to top