Molecular chaperones regulate p53 and suppress senescence programs

Michael Sherman, Vladimir Gabai, Cornelia O'Callaghan, Julia Yaglom

Research output: Contribution to journalShort surveypeer-review

36 Scopus citations


Many types of cancer cells constitutively express major molecular chaperones at high levels. Recent findings demonstrate that specific depletion of individual chaperones, including various members of the Hsp70 family, small heat shock proteins, or VCP/p97, leads to activation of p53 pathway and subsequently triggers cellular senescence. Here, we discuss a possibility that in cancer cells high levels of chaperones serve to keep the p53 signaling under control, thus allowing cancer cells to evade the default senescence and form tumors.

Original languageEnglish
Pages (from-to)3711-3715
Number of pages5
JournalFEBS Letters
Issue number19
StatePublished - 31 Jul 2007
Externally publishedYes


  • Cancer
  • Heat shock proteins
  • Hsp70
  • Mortalin
  • Senescence
  • p21
  • p53


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