Recombinant Human MIP-1 alpha/CCL3 protein (Active)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

MIP-1 alpha also known as CCL3 is a chemokine that plays a critical role in the immune system. With a molecular weight of around 8 kDa it is primarily expressed in activated T-cells macrophages and fibroblasts. MIP-1 alpha acts as a signaling protein that binds to receptors on target cells directing the movement of immune cells. Researchers commonly refer to it using various alternative names such as MIP-1a and CCL3-alpha rat and it is frequently measured using assays like MIP-1 alpha ELISA for experimental analyses.

Biological function summary

Proteins including MIP-1 alpha participate in the recruitment and activation of diverse immune cells aiding the inflammatory response. Through interaction with receptors like CCR1 and CCR5 MIP-1 alpha mobilizes cells like natural killer cells and monocytes. This chemokine does not generally form part of a larger protein complex but interacts directly with membrane receptors to exert its function in immune cell chemotaxis.

Pathways

MIP-1 alpha operates in the context of both the inflammatory response and the chemokine signaling pathways. Its involvement in these pathways helps mediate the trafficking of leukocytes. Notably MIP-1 alpha interacts with proteins such as CCR1 and CCR5 to transmit signals that instigate immune responses. These proteins are integral to its role in modulating immunity providing targets for research into controlling inflammatory processes.

MIP-1 alpha closely relates to conditions such as rheumatoid arthritis and HIV infection. In rheumatoid arthritis its overexpression can lead to excessive inflammation and joint destruction. Meanwhile in HIV infection MIP-1 alpha interacts with CCR5 a co-receptor necessary for the virus entry into cells. This dual relationship elucidates its potential as a therapeutic target in managing both inflammatory diseases and viral entry mechanisms.