Receptor Tyrosine Kinases Activate Canonical WNT/β-Catenin Signaling via MAP Kinase/LRP6 Pathway and Direct β-Catenin Phosphorylation

نویسندگان

  • Pavel Krejci
  • Anie Aklian
  • Marketa Kaucka
  • Eva Sevcikova
  • Jirina Prochazkova
  • Jan Kukla Masek
  • Pavol Mikolka
  • Tereza Pospisilova
  • Tereza Spoustova
  • MaryAnn Weis
  • William A. Paznekas
  • Joshua H. Wolf
  • J. Silvio Gutkind
  • William R. Wilcox
  • Alois Kozubik
  • Ethylin Wang Jabs
  • Vitezslav Bryja
  • Lisa Salazar
  • Iva Vesela
  • Lukas Balek
چکیده

Receptor tyrosine kinase signaling cooperates with WNT/β-catenin signaling in regulating many biological processes, but the mechanisms of their interaction remain poorly defined. We describe a potent activation of WNT/β-catenin by FGFR2, FGFR3, EGFR and TRKA kinases, which is independent of the PI3K/AKT pathway. Instead, this phenotype depends on ERK MAP kinase-mediated phosphorylation of WNT co-receptor LRP6 at Ser1490 and Thr1572 during its Golgi network-based maturation process. This phosphorylation dramatically increases the cellular response to WNT. Moreover, FGFR2, FGFR3, EGFR and TRKA directly phosphorylate β-catenin at Tyr142, which is known to increase cytoplasmic β-catenin concentration via release of β-catenin from membranous cadherin complexes. We conclude that signaling via ERK/LRP6 pathway and direct β-catenin phosphorylation at Tyr142 represent two mechanisms used by various receptor tyrosine kinase systems to activate canonical WNT signaling.

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عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2012