MYELOID NEOPLASIA Cytotoxic effects of bortezomib in myelodysplastic syndrome/acute myeloid leukemia depend on autophagy-mediated lysosomal degradation of TRAF6 and repression of PSMA1

نویسندگان

  • Jing Fang
  • Garrett Rhyasen
  • Lyndsey Bolanos
  • Christopher Rasch
  • Melinda Varney
  • Mark Wunderlich
  • Susumu Goyama
  • Gerrit Jansen
  • Jacqueline Cloos
  • Carmela Rigolino
  • Agostino Cortelezzi
  • James C. Mulloy
  • Esther N. Oliva
  • Maria Cuzzola
  • Daniel T. Starczynowski
چکیده

1Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH; 2Department of Cancer and Cell Biology, University of Cincinnati, Cincinnati, OH; Departments of 3Rheumatology and 4Pediatric Oncology/Hematology, Vrije Universiteit University Medical Center, Amsterdam, The Netherlands; 5Bone Marrow Unit, Azienda Ospedaliera, Bianchi-Melacrino-Morelli, Reggio Calabria, Italy; 6Department of Medical Sciences, Hematology 1, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico, Ca’ Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy; and 7Hematology Unit, Azienda Ospedaliera, Bianchi-Melacrino-Morelli, Reggio Calabria, Italy

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منابع مشابه

Cytotoxic effects of bortezomib in myelodysplastic syndrome/acute myeloid leukemia depend on autophagy-mediated lysosomal degradation of TRAF6 and repression of PSMA1.

Bortezomib (Velcade) is used widely for the treatment of various human cancers; however, its mechanisms of action are not fully understood, particularly in myeloid malignancies. Bortezomib is a selective and reversible inhibitor of the proteasome. Paradoxically, we find that bortezomib induces proteasome-independent degradation of the TRAF6 protein, but not mRNA, in myelodysplastic syndrome (MD...

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تاریخ انتشار 2012