Product nameHuman HO 1 ELISA Kit
See all HO 1 kits
Intra-assay Sample n Mean SD CV% Overall 30 < 10% Inter-assay Sample n Mean SD CV% Overall 30 < 10%
Sample typeSerum, Tissue Extracts, Cell Lysate
Assay typeSandwich (quantitative)
Range0.78 ng/ml - 25 ng/ml
Assay time2h 30m
Assay durationMultiple steps standard assay
Species reactivityReacts with: Human
Does not react with: Mouse, Rat
Abcam’s HO-1 in vitro ELISA (Enzyme-Linked Immunosorbent Assay) kit is designed for the accurate quantitative measurement of HO-1 in cell lysates and tissue extracts.
A mouse monoclonal antibody specific for HO-1 is pre-coated on the wells of a plate. Standards or test samples are added to the wells, incubated and then washed. A HO-1 polyclonal antibody is then added, incubated and washed. An HRP conjugated anti-IgG antibody is then added, incubated. The plate is washed once more and the TMB substrate is then added which HRP catalyzes, generating a blue coloration after incubation. A stop solution is added which generates conversion to yellow color read at 450 nm which is proportional to the amount of analyte bound.
Heme Oxygenase 1 (HO 1) also known as Hsp32, is the inducible isoform of heme oxygenase that catalyzes the NADPH, O2 and cytochrome P450 reductase dependent oxidation of heme to carbon monoxide, ferrous iron and biliverdin which is rapidly reduced to bilirubin. These products of the HO reaction have important physiological effects: carbon monoxide is a potent vasodilator and has
been implicated to be a physiological regulator of cGMP and vascular tone; biliverdin and its product bilirubin are potent antioxidants; “free” iron increases oxidative stress and regulates the expression of many mRNAs (e.g., DCT-1, ferritin and transferring receptor) by affecting the conformation of iron regulatory protein (IRP)-1 and its binding to iron regulatory elements (IREs) in the 5’- or 3’- UTRs of the mRNAs. To date, three identified heme oxygenase isoforms are part of the HO system that catalyze heme into biliverdin and carbon monoxide. These are inducible HO 1 or Hsp32, constitutive HO 2 that is abundant in the brain and testis, and HO 3 which is related to HO 2 but is the product of a different gene. The HO system is the rate-limiting step in heme degradation and HO activity decreases the levels of heme which is a well-known potent catalyst of lipid peroxidation and oxygen radical formation.
The expression of HO 1 is highly responsive to all types of stimuli that cause oxidative stress and it is up regulated during exposure to oxidants, UV-A irradiation and a series of agents including cytokines, hormones, heme and heavy metals. HO 1 is a vital component of neuronal defense mechanisms and oxidative stress has been postulated to be the underlying basis for neuronal cell death in neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease. The expression of HO 1 is normally very low in the brain but increases markedly after heat shock, ischemia or glutathione depletion. Spatial distribution of HO 1 expression in AD brain is essentially identical to that of the pathogenic conformational changes of tau protein that is the major component of the intraneuronal lesion of AD, neurofibrillary tangles.
HO 1 expression and tau expression may be regulated by oxidative stresses in a coordinated manner and play a pivitol role in the cytoprotection of neuronal cells. Plasma and cerebrospinal fluid HO 1 protein and lymphocyte HO 1 mRNA levels are decreased in subjects with sporadic AD relative to normal elderly controls suggesting that measurement of HO 1 may serve as a useful biological marker in early sporadic AD.
Oxidative stress in the heart caused by ischemia and reperfusion has been shown to lead to cardiomyocyte death. An absence of HO 1 has detrimental consequences whereas overexpression of HO 1 plays a protective role in hypoperfusion and ischemia/reperfusion-induced myocardial injury. Under normal conditions, HO 1 is present at low levels in all organs except the spleen, but its expression is rapidly accelerated in response to pathophysiological conditions such as renal ischemia/reperfusion and cellular transformation. HO 1 overexpression exerts beneficial cytoprotective effects in a number of transplantation models, including antigen-independent
ischemia/reperfusion injury, acute and chronic allograft rejection and xenotransplantation.
The mechanisms by which HO 1 confers its protective effects are currently poorly understood but this area of investigation is active and rapidly evolving. The measurement of HO 1 in various cell types, tissues and bodily fluids may provide new insights into the physiological roles of HO 1 and may lead to monitoring HO 1 levels as a biomarker for therapeutic interventions or as an environmental biomarker in toxicology studies.
Tested applicationsSuitable for: Sandwich ELISAmore details
Storage instructionsPlease refer to protocols.
Components 1 x 96 tests 20X Wash Buffer Concentrate 1 x 100ml 5X Extraction Reagent 1 x 10ml Antibody Diluent 1 x 11ml Anti-Human HO-1 1 x 25µl Anti-rabbit IgG HRP Conjugate 1 x 25µl HRP Conjugate Diluent 1 x 11ml Microplate coated with monoclonal anti-HO-1 antibody (12 x 8 wells) 1 unit Recombinant HO-1 Standard 1 x 25µl Sample Diluent 1 x 50ml Stop Solution 2 1 x 10ml TMB Substrate 1 x 10ml
RelevanceFunction: 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. Tissue specificity: Expressed at higher levels in renal cancer tissue than in normal tissue (at protein level). Disease: Heme oxygenase 1 deficiency Similarity: Belongs to the heme oxygenase family.
- Heat shock protein 32 kD
- heme oxygenase (decycling) 1
Our Abpromise guarantee covers the use of ab133064 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|Sandwich ELISA||Use at an assay dependent concentration.|
This product has been referenced in:
- Shono Y et al. Characterization of a c-Rel Inhibitor That Mediates Anticancer Properties in Hematologic Malignancies by Blocking NF-?B-Controlled Oxidative Stress Responses. Cancer Res 76:377-89 (2016). ELISA ; Human . Read more (PubMed: 26744524) »