Regulation of the nuclear proteasome activity in myelomonocytic human leukemia cells after adriamycin treatment.

Blood
O CiftciR Hass

Abstract

Treatment of different human leukemia cell variants with the anthracycline adriamycin was associated with a rapid activation of the proteasome. Thus, proliferating U937, TUR, and retrodifferentiated U937 cells exhibited a 4.3-fold, 5.8-fold, and 4.3-fold proteasome activation within 15 minutes after adriamycin treatment, respectively. In contrast, little if any proteasome activation was detectable in a growth-arrested differentiated U937 population following adriamycin treatment. Further analysis of this mechanism revealed a significant reduction of adriamycin-induced proteasome activity after inhibition of poly(ADP-ribose) polymerase (PARP) by 3-aminobenzamide (3-ABA) in the proliferating leukemic cell types. These findings suggested that PARP is involved in the regulation of drug-induced proteasome activation. Indeed, anti-PARP immunoprecipitation experiments of adriamycin-treated cells revealed increasing levels of coprecipitated, enzymatically active proteasome particularly in the proliferating cell variants in contrast to the differentiated U937 cells, with a maximum after 15 minutes, and sensitivity to PARP inhibition by 3-ABA. The specific role of the PARP was investigated in U937 and TUR cell clones stably transfected w...Continue Reading

References

Jul 11, 1992·Nucleic Acids Research·H U EnrightR P Hebbel
Jan 1, 1991·Free Radical Biology & Medicine·M Dizdaroglu
Jun 1, 1991·Environmental Health Perspectives·M NagaoT Sugimura
Sep 1, 1990·Proceedings of the National Academy of Sciences of the United States of America·A KumatoriA Ichihara
Mar 1, 1988·International Journal of Radiation Biology and Related Studies in Physics, Chemistry, and Medicine·J P Daugherty, T A Simpson
Mar 1, 1988·Experimental Cell Research·N P SinghE L Schneider
Oct 1, 1987·Photochemistry and Photobiology·P Musk, P G Parsons
Sep 1, 1994·Molecular and Cellular Biochemistry·G de MurciaJ Ménissier de Murcia
Jan 1, 1994·Methods in Enzymology·A Z Reznick, L Packer
Apr 1, 1993·Toxicology Letters·T Boulikas
Mar 8, 1996·The Journal of Biological Chemistry·S M CuttsD R Phillips
Jun 28, 1996·The Journal of Biological Chemistry·T GruneK J Davies
Jan 1, 1996·Annual Review of Biochemistry·O CouxA L Goldberg
Nov 5, 1997·International Journal of Cancer. Journal International Du Cancer·R Hass, J A Lopez-Guerrero
Aug 11, 1998·Biochemical Pharmacology·X YinY J Kang
Feb 17, 1999·Archives of Biochemistry and Biophysics·O UllrichT Grune
May 26, 1999·Proceedings of the National Academy of Sciences of the United States of America·O UllrichK J Davies
Jun 11, 1999·The Journal of Biological Chemistry·J C AméG de Murcia
Jun 12, 1999·Biochemical and Biophysical Research Communications·P Mayer-KuckukM Schweiger

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Citations

Oct 19, 2002·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·Jenny Arnold, Tilman Grune
Nov 25, 2004·Progress in Biophysics and Molecular Biology·Paul A NguewaJosé M Pérez
Jan 23, 2008·Biological Chemistry·Catharina Bertram, Ralf Hass
Apr 2, 2009·Biological Chemistry·Ralf Hass
Oct 28, 2010·Free Radical Biology & Medicine·Edina BakondiTilman Grune
Dec 23, 2009·Free Radical Biology & Medicine·Betul CatalgolTilman Grune
Aug 18, 2004·Biochemical Pharmacology·A Ivana Scovassi, Marc Diederich
Feb 22, 2012·Free Radical Biology & Medicine·José Luis García-GiménezFederico V Pallardó
Oct 15, 2003·The Journal of Pharmacology and Experimental Therapeutics·George W SmallRobert Z Orlowski
Sep 29, 2005·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Asangi R K KumarapeliXuejun Wang
Mar 5, 2008·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Eyal C AttarPhilip C Amrein
Mar 28, 2008·Science Signaling·Catharina Bertram, Ralf Hass

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