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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAqwloxfM0Vu_DUDw5-sz5zr5f58TUOUbi08slbHxj9JU#_4 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAqwloxfM0Vu_DUDw5-sz5zr5f58TUOUbi08slbHxj9JU#_3 http://www.w3.org/ns/prov#value Induction of HO-1 corresponds to a significant suppression of inflammation, whereas inhibition of the enzyme potentiates the inflammatory response in several models of inflammation (Amersi et al., 1999; Nath, 1999; Vogt et al., 1996; Agarwal and Nick, 2000; Willis et al., 2000; Wagener et al., 2001b). These include corneal, lung, and renal inflammatory models, and in transplantation biology (Laniado-Schwartzman et al., 1997; Platt and Nath, 1998; Otterbein et al., 1999a; Agarwal and Nick, 2000). View larger version (19K): [in this window] [in a new window] FIG. 6. This diagram demonstrates the intricate relationships of HO-1, TNF-, and the heme proteins iNOS and COX during inflammation in a pleurisy model. During inflammation, TNF-, COX, and iNOS get induced, adhesion molecule expression increases, and leukocytes are recruited (Willis et al., 1996, 2000; Wagener et al., 2001b). 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