Technical datasheet
Description
The monoclonal antibody 23C11 recognizes oxidized low-density lipoprotein receptor-1 (LOX-1). LOX-1 is a single-pass type II membrane protein (~45 kDa) and belongs to the C-type lectin-like protein superfamily. LOX-1 is expressed at high level in endothelial cells and vascular-rich organs such as placenta, lung, liver, brain aortic intima, bone marrow, spinal cord and substantia nigra. It is also expressed on the surface of dendritic cells.
This unique scavenger receptor LOX-1 plays important roles in atherogenesis. LOX-1 mediates the recognition, internalization and degradation of oxidatively modified low density lipoprotein (oxLDL) by vascular endothelial cells. OxLDL is a marker of atherosclerosis, inducing vascular endothelial cell activation and dysfunction, resulting in pro-inflammatory responses, pro-oxidative conditions and apoptosis. LOX-1 associates with oxLDL inducing the activation of NF-kappa-B through an increased production of intracellular reactive oxygen and a variety of pro-atherogenic cellular responses including a reduction of nitric oxide (NO) release, monocyte adhesion and apoptosis. In addition to binding oxLDL, LOX-1 acts as a receptor for the HSP70 protein involved in antigen cross-presentation to naive T-cells in dendritic cells, thereby participating in cell-mediated antigen cross-presentation. LOX-1 is involved in the inflammatory process, by acting as a leukocyte-adhesion molecule at the vascular interface in endotoxin-induced inflammation. LOX-1 also acts as a receptor for advanced glycation end (AGE) products, activated platelets, monocytes, apoptotic cells and both Gram-negative and Gram-positive bacteria.
The LOX-1 gene is a so-called immediate early gene that is dynamically modulated by several factors in vitro and in vivo. LOX-1 expression is induced by stimuli such as inflammatory cytokines, OxLDL, TNF-alpha, TGF-beta, and ANG II in vitro, and several proatherogenic factors in vivo.
Monoclonal antibody 23C11 neutralizes LOX-1 and inhibits Hsp70 binding to dendritic cells and Hsp70-induced antigen cross-presentation.
In vivo, targeting LOX-1 with a tumor antigen using anti-LOX-1 antibody 23C11 induces anti-tumor immunity.
Cross Reactivity
Cross reactant | Reactivity |
Mouse | Yes |
Immunogen
Fusion protein of extracellular domain (aa 71-273) of human LOX-1 with murine Fcγ1 (LOX-1-muFc) produced in PEAK cells
Formulation
0.5 mg (100 µg/ml) 0.2 µm filtered antibody solution in PBS (exact concentration is indicated on the label)
Species
Mouse IgG1
Application
| | F | FC1,2 | FS1,3 | IA | IF2 | IP | P | W | | Yes | | ● | ● | | ● | | | | | No | | | | | | | | | | N.D. | ● | | | ● | | ● | ● | ● | |
N.D.= Not Determined; F = Frozen sections; FC = Flow Cytometry; FS = Functional Studies; IA = Immuno Assays; IF = Immuno Fluorescence; IP = Immuno Precipitation; P = Paraffin sections; W = Western blot Application FC was tested in house by Hycult Biotech. |
Application notes
FC: 10 µg/ml antibody used on human peripheral blood myeloid DC and macrophages FS: antibody totally prevented Hsp70 binding to LOX-1-CHO but not mock-transfected CHO cells (Ref 1)
Use
For flow cytometry dilutions to be used depend on detection system applied. It is recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:50. For functional studies,
in vitro dilutions have to be optimized in user's experimental settting.
Aliases
Lectin-like oxidized LDL receptor 1, Ox-LDL receptor 1, C-type lectin domain family 8 member A
Positive control
Human APCs
Storage and stability
Product should be stored at 4°C. Under recommended storage conditions, product is stable for one year.
References
1. Delneste, Y et al; Involvement of LOX-1 in dendritic cell-mediated antigen cross-presentation. Immunity 2002, 17: 353
2. Jeannin, P et al; Complexity and complementarity of outer membrane protein A recognition by cellular and humoral innate immunity receptors. Immunity 2005, 22: 551
3. Parlato, S et al; LOX-1 as a natural IFN-α-mediated signal for apoptotic cell uptake and antigen presentation in edndritic cells. Blood 2010, 115: 1554
Precautions
For research use only. Not for use in or on humans or animals or for diagnostics. It is the responsibility of the user to comply with all local/state and Federal rules in the use of this product. Hycult Biotech is not responsible for any patent infringements that might result with the use or derivation of this product.
Also available
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HM2122
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CD36, Human, mAb FA6-152
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HM2122BT
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CD36, Human, mAb FA6-152, biotinylated
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HM2122F
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CD36, Human, mAb FA6-152, FITC
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HM2138BT
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LOX-1, Human, mAb 23C11, biotinylated
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HM2138F
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LOX-1, Human, mAb 23C11, FITC
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References
1. Delneste, Y et al; Involvement of LOX-1 in dendritic cell-mediated antigen cross-presentation. Immunity 2002, 17: 353
2. Jeannin, P et al; Complexity and complementarity of outer membrane protein A recognition by cellular and humoral innate immunity receptors. Immunity 2005, 22: 551
3. Parlato, S et al; LOX-1 as a natural IFN-α-mediated signal for apoptotic cell uptake and antigen presentation in edndritic cells. Blood 2010, 115: 1554
Scientific info
Knocking out LOX-1 limits myocardial ischemia-reperfusion injury in mice.
Lectin-like oxidized low-density lipoprotein receptors (e.g LOX-1) are upregulated during myocardial ischemia-reperfusion, and appear to be associated with apoptosis, necrosis, and left ventricular functional deterioration. A recent study with LOX-1 knock-out mice shows that “taking away” LOX-1 expression limits myocardial ischemia-reperfusion injury.
Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), a member of the C-type lectin-like protein superfamily, is a key modulator of myocardial ischemia-reperfusion (I-R) injury, and its effect is mediated by pro-oxidant signals.
This is the outcome of a recent study in which the pathogenic role of LOX-1 in the determination of I-R injury to the heart was tested. For this purpose, researchers subjected LOX-1 knockout mice to 60 min of left coronary artery occlusion followed by 60 min of reperfusion. Compared to wild-type mice, knock-outs showed preservation of cardiac function, less lipid peroxidation and attenuated myocardial inflammatory response (e.g. decreased expression of nitrotyrosine and indicuble nitric oxide synthase (iNOS)).
In an earlier study researchers of this group showed that treatment of rats with a specific antibody to LOX-1 before ischemia reduced I-R injury.
The combined results from both animal studies suggest that LOX-1 may serve as a potential therapeutic target for myocardial ischemic injury.
References:
1. Hu, C et al; LOX-1 abrogation reduces myocardial ischemia-reperfusion injury in mice. J Mol Cell Cardiol 2007, Oct 23, Epub ahead of print
2. Li, D et al; Expression of lectin-like oxidized low-density lipoprotein receptors during ischemia-reperfusion and its role in determination of apoptosis and left ventricular dysfunction. J Am Coll Cardiol 2003, 41:1048