title: Enhanced redox factor 1 (REF1)-modulated p53 stabilization and JNK1 dissociation in response to selenomethionine.
abstract: OBJECTIVE
  p53 is reportedly activated without any genotoxicity through redox modulation of redox factor 1 (REF1). REF1 is documented to modulate the redox status under selenomethionine (SeMet). In this study, we investigated the mechanism of p53 stabilization by SeMet.
  
  
  METHODS
  We mainly used ubiquitination assay and immunoprecipitation to determine the potential role of REF1 and c-jun N-terminal kinase 1 (JNK) in modulation of p53 stabilization by SeMet.
  
  
  RESULTS
  The amount of ubiquitinated p53 decreased significantly under SeMet treatment, suggesting that SeMet might inhibit the proteasome-dependent degradation of p53. In addition, we observed that JNK was considerably associated with p53 in REF1 siRNA-treated cells, implying a possible role for SeMet-induced REF1 activity in modulation of the interaction between JNK and p53 via changes in p53 redox status.
  
  
  CONCLUSIONS
  Our results suggest that the alternate mechanism of p53 stabilization by SeMet might provide an important clue in elucidating the molecular mechanism of chemopreventative compounds against various oxidative stresses.
authors.affiliation: Department of Life Science, Dongguk University, 30 Pildong-ro 1-gil, Jung-gu, Seoul 100-715, Republic of Korea, seoyr@dongguk.edu.
authors.forename: Hwa Jin
authors.initials: HJ
authors.lastname: Jung
authors.forename: Hye Lim
authors.initials: HL
authors.lastname: Kim
authors.forename: Young Rok
authors.initials: YR
authors.lastname: Seo
mesh_terms: D045744:Cell Line, Tumor; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000378:metabolism*; D006801:Humans; D048055:Mitogen-Activated Protein Kinase 8 / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012645:Selenomethionine / Q000494:pharmacology*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D054875:Ubiquitination
chemical_list: D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; D012645:Selenomethionine; D048055:Mitogen-Activated Protein Kinase 8; C085108:APEX1 protein, human; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase
keywords: JNK; cancer prevention; p53; protein stability; redox factor 1; selenomethionine; ubiquitination