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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/RAAcP3jgD1aXDXwCw-XQnvj1waWebDAhMn8wDqwrdkZUE#_4 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAAcP3jgD1aXDXwCw-XQnvj1waWebDAhMn8wDqwrdkZUE#_3 http://www.w3.org/ns/prov#value , whereas Rucker et al. (2001) observed in vivo decreased ICAM-1 expression in a model of arterial injury when HO-1 was up-regulated prior to injury. This model may thus provide a plausible molecular basis for the previously reported anti-inflammatory properties of HO-1. The HO-2 and HO-3 isoforms probably function normally as first defense against oxidative/inflammatory insults, whereas upon stress HO-1 is swiftly up-regulated and strongly protects against further injurious signals. HO-2, which is highly expressed in brains and testis, protects, e.g., neurons against oxidative stress. HO-2 may function as a physiologic regulator of cellular function, whereas HO-1 plays a role in modulating tissue responses to injury in pathophysiologic states (Wagener et al., 1999). 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