CCL4/MIP-1 beta Products
CCL4/MIP-1 beta is a beta chemokine that is secreted at sites of inflammation by activated leukocytes, lymphocytes, vascular endothelial cells, and pulmonary smooth muscle cells. It attracts a variety of immune cells to sites of microbial infection as well as to other pathologic inflammation such as allergic asthma and ischemic myocardium. CCL4 is secreted from activated monocytes as a heterodimer with CCL3/MIP-1 alpha. It signals through CCR5, and an N-terminally trimmed form additionally interacts with CCR1 and CCR2. In humans, the ability of CCL4 to bind CCR5 inhibits the cellular entry of M-tropic HIV-1 which utilizes CCR5 as a coreceptor.
5 results for "CCL4/MIP-1 beta" in Products
5 results for "CCL4/MIP-1 beta" in Products
CCL4/MIP-1 beta Products
CCL4/MIP-1 beta is a beta chemokine that is secreted at sites of inflammation by activated leukocytes, lymphocytes, vascular endothelial cells, and pulmonary smooth muscle cells. It attracts a variety of immune cells to sites of microbial infection as well as to other pathologic inflammation such as allergic asthma and ischemic myocardium. CCL4 is secreted from activated monocytes as a heterodimer with CCL3/MIP-1 alpha. It signals through CCR5, and an N-terminally trimmed form additionally interacts with CCR1 and CCR2. In humans, the ability of CCL4 to bind CCR5 inhibits the cellular entry of M-tropic HIV-1 which utilizes CCR5 as a coreceptor.
Assay Range: | 15.6 - 1,000 pg/mL |
Applications: | ELISA |
Reactivity: | Human |
Details: | Mouse IgG2b Monoclonal Clone #24006 |
Applications: | WB, CyTOF-ready, ICFlow, Neut |
Source: | E. coli |
Accession #: | P13236.1 |
Applications: | BA |
Reactivity: | Human |
Details: | Goat IgG Polyclonal |
Applications: | WB, IHC, ICC, Neut |
Luminex High Performance Assays go through rigorous development, validation, and quality control testing to ensure you are getting the best performance out of your multiplex assay. Panels are customizable so you can order a selection of the analytes or the entire panel.