Elsevier

Methods in Enzymology

Volume 300, 1999, Pages 345-363
Methods in Enzymology

Inhibition of NF-κB activation in vitro and in vivo: Role of 26S proteasome

https://doi.org/10.1016/S0076-6879(99)00140-8Get rights and content

Abstract

The results observed with PS-273 have also been demonstrated with other boronic acid proteasome inhibitors, as well as the peptide aldehyde and lactacystin class of proteasome inhibitors. The relative potencies for inhibition in the above mentioned assays correlates generally with Ki values for proteasome inhibition. This is evidence that the intracellular mode of action of the inhibitors is indeed through proteasome inhibition.

References (47)

  • M. Grilli et al.

    Int. Rev. Cytol.

    (1993)
  • P.A. Baeuerle et al.

    Cell

    (1996)
  • M. Hochstrasser

    Curr. Opin. Biol.

    (1995)
  • A. Ciechanover

    Cell

    (1994)
  • M. Scheffner et al.

    Cell

    (1993)
  • D. Shkedy et al.

    FEBS Lett.

    (1994)
  • A. Murray

    Cell

    (1995)
  • J. Adams et al.

    Ann. Reports Med. Chem.

    (1996)
  • A.L. Goldberg et al.

    Chemistry & Biology

    (1995)
  • M. Chu-Ping et al.

    J. Biol. Chem.

    (1994)
  • M.A. Read et al.

    Immunity

    (1995)
  • P.J. Barnes et al.

    New. Eng. J. Med.

    (1997)
  • A.S. Baldwin

    Annu. Rev. Immunol.

    (1996)
  • D. Thanos et al.

    Cell

    (1995)
  • V.J. Palombella et al.

    Cell

    (1994)
  • N. Auphan et al.

    Science

    (1995)
  • E. Kopp et al.

    Science

    (1994)
  • R. Scheinman et al.

    Science

    (1995)
  • Z. Chen et al.

    Genes & Develop.

    (1995)
  • D.C. Scherer et al.
  • J. DiDonato et al.

    Mol. Cell. Biol.

    (1996)
  • M. Rolfe et al.
  • I. Stancovski et al.

    Mol. Cell. Biol.

    (1995)
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