anti-4-Hydroxy-2-nonenal [4-HNE], mAb (HNEJ-2)
|Product Type||Monoclonal Antibody|
|Immunogen/Antigen||4-Hydroxy-2-nonenal (4-HNE) modified keyhole limpet hemocyanin.|
Immunohistochemistry: Recommended concentration is 25μg/mL
Western Blot: Recommended concentration is 15μg/mL
|Specificity||Recognizes 4-HNE-lysine, 4-HNE-histidine and 4-HNE cysteine adduct. Has much higher affinity for the 4-HNE-histidine adduct than 4-HNE-lysine or 4-HNE cysteine adduct. Shows almost negligible reactivity with proteins that were treated with other aldehydes, such as 2-nonenal, 2-hexenal, 1-hexanal, 4-hydroxy-2-hexenal, formaldehyde, or glutaraldehyde.|
|Purity Detail||Ammonium sulfate purified.|
|Formulation||Lyophilized. Contains 50mM Tris-buffered saline (TBS).|
|Reconstitution||Reconstitute with 1000μL of distilled water.|
|Other Product Data||
Click here for Original Manufacturer Product Datasheet
Our product description may differ slightly from the original manufacturers product datasheet.
|Declaration||Manufactured by JaICA.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
|Handling Advice||Avoid freeze/thaw cycles.|
Stable for at least 3 years after receipt when stored at -20°C.
After reconstitution, prepare aliquots and store at -20°C.
|Product Specification Sheet|
Reactive oxygen species (ROS) are involved in lipid peroxidation inside the living bodies, and membrane lipids are one of the major targets of ROS. During the peroxidation process, a variery of aldehydes are formed. 4-hydroxy-2-nonenal (4-HNE) is an alpha, beta unsaturated aldehyde that can be formed by peroxidation of omega-6 unsaturated fatty acids such as linoleic acid and arachidonic acid. Especially, 4-HNE formed inside living body is reported to originate from phospholipid-bound arachidonic acid. 4-HNE may be one of the most reliable biomarker of lipid peroxidation.
- The monclonal antibody specific for the 4-hydroxy-2-nonenal histidine adduct: S.Toyokuni, et al.; FEBS Lett. 359, 189 (1995) [Western blot]
- Induction and nuclear translocation of thioredoxin by oxidative damage in the mouse kidney: independence of tubular necrosis and sulfhydryl depletion: T. Tanaka, et al.; Lab. Invest. 77, 145 (1997)