Mouse CD5 Antigen-Like (CD5L) ELISA KitIMSCD5LKT
This Mouse CD5 Antigen-Like (CD5L) ELISA Kit from Innovative Research is intended for quantitative detection of activated mouse CD5L in cell culture supernates, cell lysates, serum and plasma (heparin, EDTA). Strip well format. Reagents for up to 96 tests.
This mouse CD5L ELISA Kit was based on standard sandwich enzyme-linked immune-sorbent assay technology. A monoclonal antibody from rat specific for CD5L has been precoated onto 96-well plates. Standards(NSO, E22-V352) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for CD5L is added subsequently and then followed by washing with PBS or TBS buffer. Avidin-Biotin-Peroxidase Complex was added and unbound conjugates were washed away with PBS or TBS buffer. HRP substrate TMB was used to visualize HRP enzymatic reaction. TMB was catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the mouse CD5L amount of sample captured in plate.
- Detection Target: CD5 Antigen-Like (CD5L)
- Uniprot ID: Q9QWK4)
- Reactivity: Mouse
- Cross-Reactivity: There is no detectable cross-reactivity with other relevant proteins.
- Range: 156pg/ml-10000pg/ml
- Sensitivity: <10pg/ml
- Storage Conditions: Store at 4?C for 6 months, at -20?C for 12 months. Avoid multiple freeze-thaw cycles. (Shipped with wet ice)
Additional Information: The capture antibody is a polyclonal antibody from goat, the detection antibody is a biotinylated polyclonal antibody from goat. Expression system for standard: CD5 antigen-like, also known as Sp alpha and AIM, is a protein that in humans is encoded by the CD5L gene. It is mapped to 1q21-q23 by fluorescence in situ hybridization. It is found that Aim expression is induced in mouse macrophages in response to loading with highly oxidized low density lipoprotein (oxLDL), and that Aim is expressed in foam cells within atherosclerotic lesions. Both the expression of Aim in lesions and its induction by oxLDL require Lxr /Rxr heterodimers. Aim-null macrophages are highly susceptible to oxLDL-induced apoptosis in vitro and undergo accelerated apoptosis in atherosclerotic lesions in vivo. Double knockout of Aim and Ldlr reduce atherosclerotic lesions. Therefore, it is concluded that AIM expression protects macrophages from apoptosis within atherosclerotic lesions, promoting early lesion development.; Immunogen sequence: 369
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