ELISA Kits - Cellular Stress, Heat Shock Proteins (HSP), Oxidative Stress

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Product Name: HO-1 StressXpress® ELISA Kit
Catalog #: SKT-111-480
Alternative Names: Heme oxygenase 1, Hemox, HMOX1, HO1, Hsp32
Size: 5x96-well
Type: ELISA
Description: ELISA kit used to quantitate the HO-1 concentration in samples
Species Reactivity: Human
Sample Type: Cell lysates, tissue extracts, serum samples
Incubation Time: 30 minutes
Sensitivity: 0.21 ng/mL
Assay Range: 0.781-50 ng/mL
Storage Temp: 4°C
Shipping Temp: Blue Ice, 4°C
Price: $1,996.00 USD Add to Cart Bulk Quote

HO-1 ELISA Kit Catalog # SKT-111 (96 well kit)	Download.pdf
HO-1 ELISA Kit Catalog # SKT-111 MSDS	Download.pdf

Research Background: Heme-oxygenase is a ubiquitous enzyme that catalyzes the initial and rate-limiting steps in heme catabolism yielding equimolar amounts of biliverdin, iron and carbon monoxide. Biliverdin is subsequently converted to bilirubin and the free iron is sequestered to ferritin (1). These products have important physiological effects as carbon monoxide is a potent vasodilator; biliverdin and bilirubin are potent antioxidants; and the free iron increases oxidative stress and regulates the expression of many mRNAs (2).
There are three isoforms of heme-oxygenase, HO-1, HO-2 and HO-3; however HO-1 and HO-2 are the major isoforms as they both have been identified in mammals (3). HO-1, also known as heat shock protein 32, is an inducible isoform activated by most oxidative stress inducers, cytokines, inflammatory agents and heat shock. HO-2 is a constitutive isoform which is expressed under homeostatic conditions. HO-1 is also considered to be a cytoprotective factor in that free heme is highly reactive and cytotoxic, and secondly, carbon monoxide is a mediator inhibiting the inflammatory process and bilirubin is a scavenger for reactive oxygen, both of which are the end products of heme catalyzation (4). It has also been shown that HO-1 deficiency may cause reduced stress defense, a pro-inflammatory tendency (5), susceptibility to atherosclerotic lesion formation (6), endothelial cell injury, and growth retardation (7). Up-regulation of HO-1 is therefore said to be one of the major defense mechanisms of oxidative stress (4).
References: 1. Froh M. et al. (2007) World J. Gastroentereol 13(25): 3478-86.
2. Elbirt K.K. and Bonkovsky H.L. (1999) Proc Assoc Am Physicians 111(5): 348-47.
3. Maines M.D., Trakshel G.M., and Kutty R.K. (1986) J Biol Chem 261: 411–419.
4. Brydun A., et al. (2007) Hypertens Res 30(4): 341-8.
5. Poss K.D. and Tonegawa S. (1997). Proc Natl Acad Sci U S A. 94: 10925–10930.
6. Yet S.F., et al. (2003) FASEB J. 17: 1759–1761.
7. Yachie A., et al. (1999) J Clin Invest. 103: 129–135.

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