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M211596200v1
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Papers In Press, published online ahead of print March 6, 2003
J. Biol. Chem, 10.1074/jbc.M211596200
Submitted on November 13, 2002
Revised on February 24, 2003
Accepted on March 6, 2003

Glutathione S-transferase omega 1-1 is a target of cytokine release inhibitory drugs and may be responsible for their effect on interleukin-1beta posttranslational processing

Ronald E. Laliberte, David G. Perregaux, Lise R. Hoth, Philip J. Rosner, Crystal K. Jordan, Kevin M. Peese, James F. Eggler, Mark A. Dombroski, Kieran F. Geoghegan, and Christopher A. Gabel

Department of Antibacterials, Immunology and Inflammation, Pfizer Global Reseach and Development, Groton, CT 06340

Corresponding Author: christopher_a_gabel{at}groton.pfizer.com

Stimulus-induced posttranslational processing of human monocyte interleukin-1beta (IL-1beta ) is accompanied by major changes to the intracellular ionic environment, activation of caspase-1, and cell death. Certain diarylsulfonylureas inhibit this response, and are designated cytokine release inhibitory drugs (CRIDs). CRIDs arrest activated monocytes so that caspase-1 remains inactive and plasma membrane latency is preserved. Affinity labeling with [14C]CRIDs and affinity chromatography on immobilized CRID were used in seeking potential protein targets of their action. Following treatment of intact human monocytes with an epoxide-bearing [14C]CRID, GST Omega 1-1 was identified as a preferred target. Moreover, labeling of this polypeptide correlated with irreversible inhibition of ATP-induced IL-1beta posttranslational processing. When extracts of human monocytic cells were chromatographed on a CRID affinity column, GST Omega 1-1 bound selectively to the affinity matrix and was eluted by soluble CRID. Recombinant GST Omega 1-1 readily incorporated [14C]CRID epoxides, but labeling was negated by co-incubation with S-substituted glutathiones or by mutagenesis of the catalytic center Cys32 to alanine. Peptide mapping by HPLC-mass spectrometry also demonstrated that Cys32 was the site of modification. Although S-alkylglutathiones did not arrest ATP-induced IL-1beta posttranslational processing or inhibit [14C]CRID incorporation into cell-associated GST Omega 1-1, a glutathione-CRID adduct effectively demonstrated these attributes. Therefore, the ability of CRIDs to arrest stimulus-induced IL-1beta posttranslational processing may be attributable to their interaction with GST Omega 1-1.


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