Tsui Fen Chou

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Specific inhibition of p97/VCP ATPase and kinetic analysis demonstrate interaction between D1 and D2 ATPase domains
    Tsui Fen Chou
    Division of Medical Genetics, Department of Pediatrics, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA 90502, USA Electronic address
    J Mol Biol 426:2886-99. 2014
  2. pmc Structure-activity relationship study reveals ML240 and ML241 as potent and selective inhibitors of p97 ATPase
    Tsui Fen Chou
    Division of Biology and Howard Hughes Medical Institute, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA
    ChemMedChem 8:297-312. 2013
  3. pmc Reversible inhibitor of p97, DBeQ, impairs both ubiquitin-dependent and autophagic protein clearance pathways
    Tsui Fen Chou
    Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA
    Proc Natl Acad Sci U S A 108:4834-9. 2011
  4. pmc Development of p97 AAA ATPase inhibitors
    Tsui Fen Chou
    Division of Biology, California Institute of Technology, Pasadena, CA, USA
    Autophagy 7:1091-2. 2011
  5. pmc Evaluating p97 inhibitor analogues for their domain selectivity and potency against the p97-p47 complex
    Chen Jie Fang
    Division of Medical Genetics, Department of Pediatrics, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, 1124 West Carson Street, Torrance, CA 90502 USA School of Chemical Biology and Pharmaceutics, Capital Medical University, Beijing 100069 P R China
    ChemMedChem 10:52-6. 2015
  6. pmc Quantitative cell-based protein degradation assays to identify and classify drugs that target the ubiquitin-proteasome system
    Tsui Fen Chou
    Division of Biology, California Institute of Technology, Pasadena, California 91125, USA
    J Biol Chem 286:16546-54. 2011
  7. pmc Altered cofactor regulation with disease-associated p97/VCP mutations
    Xiaoyi Zhang
    Division of Medical Genetics, Department of Pediatrics, Harbor UCLA Medical Center, Los Angeles Biomedical Research Institute, Torrance, CA 90502 College of Pharmaceutical Sciences, Capital Medical University, Beijing 100069, People s Republic of China
    Proc Natl Acad Sci U S A 112:E1705-14. 2015

Collaborators

  • Yanzhuang Wang
  • Xiaoyi Zhang
  • Lin Gui
  • Chen Jie Fang
  • Henry J Lin
  • Michelle R Arkin
  • Michelina Iacovino
  • Conrad C Weihl
  • Frank J Schoenen
  • Derek R Moen
  • Youjin Lee
  • Daniel E Wong
  • Lynn Lehmann
  • Pei Yin Shih
  • Kelin Li
  • Xiaoyan Zhang
  • James Siho Lee
  • Kevin J Frankowski
  • Stacie L Bulfer
  • Valentina Sanghez

Detail Information

Publications7

  1. pmc Specific inhibition of p97/VCP ATPase and kinetic analysis demonstrate interaction between D1 and D2 ATPase domains
    Tsui Fen Chou
    Division of Medical Genetics, Department of Pediatrics, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA 90502, USA Electronic address
    J Mol Biol 426:2886-99. 2014
    ..These differential effects provide the first evidence that p97 cofactors and disease mutations can alter p97 inhibitor potency and suggest the possibility of developing context-dependent inhibitors of p97. ..
  2. pmc Structure-activity relationship study reveals ML240 and ML241 as potent and selective inhibitors of p97 ATPase
    Tsui Fen Chou
    Division of Biology and Howard Hughes Medical Institute, California Institute of Technology, 1200 East California Boulevard, Pasadena, CA 91125, USA
    ChemMedChem 8:297-312. 2013
    ..Our results nominate ML240 as a promising starting point for the development of a novel agent for the chemotherapy of cancer, and provide a rationale for developing pathway-specific p97 inhibitors...
  3. pmc Reversible inhibitor of p97, DBeQ, impairs both ubiquitin-dependent and autophagic protein clearance pathways
    Tsui Fen Chou
    Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA
    Proc Natl Acad Sci U S A 108:4834-9. 2011
    ..DBeQ also potently inhibits cancer cell growth and is more rapid than a proteasome inhibitor at mobilizing the executioner caspases-3 and -7. Our results provide a rationale for targeting p97 in cancer therapy...
  4. pmc Development of p97 AAA ATPase inhibitors
    Tsui Fen Chou
    Division of Biology, California Institute of Technology, Pasadena, CA, USA
    Autophagy 7:1091-2. 2011
    ....
  5. pmc Evaluating p97 inhibitor analogues for their domain selectivity and potency against the p97-p47 complex
    Chen Jie Fang
    Division of Medical Genetics, Department of Pediatrics, Harbor UCLA Medical Center and Los Angeles Biomedical Research Institute, 1124 West Carson Street, Torrance, CA 90502 USA School of Chemical Biology and Pharmaceutics, Capital Medical University, Beijing 100069 P R China
    ChemMedChem 10:52-6. 2015
    ..These results highlight the possibility of developing domain-selective and complex-specific p97 inhibitors in order to further elucidate the physiological roles of p97 and its cofactors. ..
  6. pmc Quantitative cell-based protein degradation assays to identify and classify drugs that target the ubiquitin-proteasome system
    Tsui Fen Chou
    Division of Biology, California Institute of Technology, Pasadena, California 91125, USA
    J Biol Chem 286:16546-54. 2011
    ..Our work establishes a high-throughput screening-compatible pipeline for identification and classification of small molecules, cDNAs, or siRNAs that target components of the ubiquitin-proteasome system...
  7. pmc Altered cofactor regulation with disease-associated p97/VCP mutations
    Xiaoyi Zhang
    Division of Medical Genetics, Department of Pediatrics, Harbor UCLA Medical Center, Los Angeles Biomedical Research Institute, Torrance, CA 90502 College of Pharmaceutical Sciences, Capital Medical University, Beijing 100069, People s Republic of China
    Proc Natl Acad Sci U S A 112:E1705-14. 2015
    ..Our results show that cofactors play a critical role in controlling p97 ATPase activity, and suggest that lack of cofactor-regulated communication may contribute to p97-associated disease pathogenesis. ..