Mitochondrial ClpP-Mediated Proteolysis Induces Selective Cancer Cell Lethality

Jo Ishizawa, Sarah F. Zarabi, R. Eric Davis, Ondrej Halgas, Takenobu Nii, Yulia Jitkova, Ran Zhao, Jonathan St-Germain, Lauren E. Heese, Grace Egan, Vivian R. Ruvolo, Samir H. Barghout, Yuki Nishida, Rose Hurren, Wencai Ma, Marcela Gronda, Todd Link, Keith Wong, Mark Mabanglo, Kensuke KojimaGautam Borthakur, Neil MacLean, Man Chun John Ma, Andrew B. Leber, Mark D. Minden, Walid Houry, Hagop Kantarjian, Martin Stogniew, Brian Raught, Emil F. Pai, Aaron D. Schimmer, Michael Andreeff

Research output: Contribution to journalArticlepeer-review

154 Citations (Scopus)


Ishizawa et al. report that hyperactivating the mitochondrial caseinolytic protease P (ClpP)degrades respiratory chain proteins, disrupts mitochondrial function, and selectively kills cancer cells, regardless of p53 status. They identify imipridones as hyperactivators of ClpP and show their anti-tumor activity.

Original languageEnglish
Pages (from-to)721-737.e9
JournalCancer Cell
Issue number5
Publication statusPublished - May 13 2019
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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