Induction of MAP kinase phosphatase 3 through Erk/MAP kinase activation in three oncogenic Ras (H-, K- and N-Ras)-expressing NIH/3T3 mouse embryonic fibroblast cell lines

Jae Hyung Koo, Sen Wang, Na Na Kang, Sun Jin Hur, Young Yil Bahk

Research output: Contribution to journalArticlepeer-review

Abstract

Ras oncoproteins are small molecular weight GTPases known for their involvement in oncogenesis, which operate in a complex signaling network with multiple effectors. Approximately 25% of human tumors possess mutations in a member of this family. The Raf1/MEK/Erk1/2 pathway is one of the most intensively studied signaling mechanisms. Different levels of regulation account for the inactivation of MAP kinases by MAPK phosphatases in a cell type- and stimuli-dependent manner. In the present study, using three inducible Ras-expressing NIH/3T3 cell lines, we demonstrated that MKP3 upregulation requires the activation of the Erk1/2 pathway, which correlates with the shutdown of this pathway. We also demonstrated, by applying pharmacological inhibitors and effector mutants of Ras, that induction of MKP3 at the protein level is positively regulated by the oncogenic Ras/Raf/MEK/Erk1/2 signaling pathway.

Original languageEnglish
Pages (from-to)370-375
Number of pages6
JournalBMB Reports
Volume49
Issue number7
DOIs
StatePublished - 2016

Bibliographical note

Publisher Copyright:
© 2016 by the The Korean Society for Biochemistry and Molecular Biology.

Keywords

  • Effector mutants
  • Mitogen- activated protein kinase phosphatase 3
  • Mitogen-activated protein kinase
  • Oncogenic Ras
  • Oncogenic Ras inducible NIH/3T3 cells

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