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HAF017). For additional reference, recombinant human HO-1 and HO-2 (5 ng/lane) were included. A specific band for HO-1/HMOX1/HSP32 was detected at approximately 32 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 2." class="big_lightbox" target="_blank">
HAF109). This experiment was conducted under reducing conditions and using the 12-230 kDa separation system." class="big_lightbox" target="_blank">
HAF017). A specific band was detected for HO-1/HMOX1/HSP32 at approximately 32 kDa (as indicated) in the parental HeLa cell line, but is not detectable in knockout HeLa cell line. GAPDH (Catalog # AF5718) is shown as a loading control. This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1." class="big_lightbox" target="_blank">
Stressed mammalian cells up-regulate heme oxygenase 1 (HO-1), which catabolizes heme to biliverdin, carbon monoxide, and free iron. Results provide genetic evidence that up-regulation of HO-1 serves as an adaptive mechanism to protect cells from oxidative damage during stress (1). When cells are injured they release their contents, resulting in a local accumulation of free heme proteins and heme. HO-1 plays a crucial role in the inflammatory process during wound healing (2). TNFalpha accelerates inflammatory responses by down-regulating HO-1 expression in human monocytes. TNF antagonists may block this TNF-dependent suppression of HO-1 expression, resulting in an amelioration of inflammation (3).