|Reactivity||Human, Mouse, Rat|
|Calculated MW||32819 Da|
|Other Names||Heme oxygenase 1, HO-1, HMOX1, HO, HO1|
|Target/Specificity||A synthetic peptide corresponding to residues surrounding the N-terminus of human HO-1 was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Heme Oxygenase-1 (HO-1) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Heme oxygenase cleaves the heme ring at the alpha methene bridge to form biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. Under physiological conditions, the activity of heme oxygenase is highest in the spleen, where senescent erythrocytes are sequestrated and destroyed. Exhibits cytoprotective effects since excess of free heme sensitizes cells to undergo apoptosis.|
|Cellular Location||Microsome. Endoplasmic reticulum membrane; Peripheral membrane protein; Cytoplasmic side|
|Tissue Location||Expressed at higher levels in renal cancer tissue than in normal tissue (at protein level)|
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Provided below are standard protocols that you may find useful for product applications.
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).
1. Poss KD, et al. Proc Natl Acad Sci USA 94(20):10925-30, 1997.
2. Wagener FA, et al. Blood 102(2):521-8, 2003.
3. Kirino Y, et al. Arthritis Rheum 56(2):464-475, 2007.
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