Mouse CCL4/MIP-1 Beta ELISA Kit

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Testing Principle：

This ELISA kit utilizes the double-antibody sandwich technique, where a microplate is coated with anti-mouse CCl4 monoclonal antibody. The sample is added onto the plate, where it binds to the fixed antibody, and then unbound components are washed away. A biotin-labeled anti-mouse CCl4 polyclonal antibody is added to the plate, and it binds to the CCl4 that has been captured by the first antibody. Another washing step is done to remove the unbound components. Then, a streptavidin-labeled horseradish peroxidase is added to the plate, and it specifically binds to the biotin. A final washing step is done to remove free components, and a substrate solution is added to promote a color change of the solution from colorless to blue. A stop solution is added, which turns the solution yellow and halts the color change process. Finally, the absorbance of the solution is measured using a microplate analyzer.

Detection type：Double sandwich enzyme immunoassay

Form: pre-coated 96-well plate

Sample type: Cell culture supernatant, Serum, Plasma

Sample quantity：100ul

Kit composition：

The components included in this kit are a 96-well polystyrene microplate coated with capture antibody, a standard, an antibody for detecting mouse CCL4, a dilution buffer, color reagents A and B, a scrubbing solution, a stop buffer, SA-HRP, and a sealing plate membrane.
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Sensitivity： 8.3 pg/mL

Detection range：15.6 - 1,000 pg/mL

Recovery rate：85.0-108.9%

Storage：2-8℃

The standard curve

Background：

MIP-1 Beta, also known as CCL4, is a type of β-chemokine that is produced by various cells in our body, including white blood cells, lymphocytes, vascular endothelial cells, and lung smooth muscle cells. This chemokine plays a crucial role in attracting different types of immune cells to the sites of infection and inflammation caused by various pathologies including allergic asthma and ischemic myocardium. It is closely related to another chemokine called CCL3 or MIP-1α, as they both exist as dimers and are secreted by activated monocytes.
The main mechanism of action for CCL4 is its ability to signal through CCR5 and, to a lesser extent, CCR1 and CCR2. The N-terminal pruning form of this chemokine is particularly effective in interacting with these receptors, which then results in the recruitment of various immune cells to the inflammation site. In fact, CCR5-dependent signaling is so critical for the immune cell response that some viruses, such as M-directional HIV-1, that use CCR5 as a co-receptor can be blocked by CCL4.
Overall, CCL4's ability to attract immune cells to sites of inflammation is crucial for mounting an effective response against infections and pathologic conditions.

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