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MIP-1α/CCL3
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q5QNW0 |
|---|---|
| Species | Mouse |
| Sequence | Ala24-Ala92 |
| Purity | > 95% as analyzed by SDS-PAGE > 95% as analyzed by HPLC |
| Endotoxin Level | < 0.2 EU/ µg of protein by gel clotting method |
| Biological Activity | The EC50 value of mouse MIP-1α/CCL3 on Ca2+ mobilization assay in CHO-K1/Gα15/mCCR1 cells (human Gα15 and mouse CCR1 stably expressed in CHO-K1 cells) is less than 100.0 ng/ml. |
| Expression System | HEK 293 |
| Formulation | Lyophilized after extensive dialysis against PBS. |
| Reconstitution | It is recommended that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Reconstitute the lyophilized powder in ddH₂O or PBS up to 100 µg/ml. |
| Storage & Stability | Upon receiving, this product remains stable for up to 6 months at lower than -70°C. Upon reconstitution, the product should be stable for up to 1 week at 4°C or up to 3 months at -20°C. For long term storage it is recommended that a carrier protein (example 0.1% BSA) be added. Avoid repeated freeze-thaw cycles. |
| Target Background | MIP-1 Alpha, also known as CCL3, G0S19-1 and SCYA3, LD78 alpha, is an inflammatory chemokine. MIP-1α belongs to the CCL chemokine family, and shares 68% homology with MIP-1β. The mature form of MIP-1α contains 69 amino acids, exists as dimers in solution, and tends to undergo reversible aggregation. It binds to CCR1, CCR4 and CCR5, and participates in the host response to invading pathogens by regulating the trafficking and activation of inflammatory cells, such as macrophages, lymphocytes, NK cells and dendritic cells. MIP-1 alpha polymorphisms are associated with HIV susceptibility or resistance. Recombinant MIP-1 alpha induces a dose-dependent inhibition of HIV and SIV infection. Upon stimulation by endogenous and exogenous agents such as Interleukin-1β, Interferon-γ, and lipoteichoic acid from gram-positive bacteria, monocytes are able to secrete significant amounts of MIP-1α. MIP-1α augments the adhesions of T lymphocytes, monocytes, and neutrophils to vascular cell adhesion molecule 1. Additionally, in wounds, MIP-1α chemoattracts macrophages in order to accelerate the tissue repair process. |
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Research Areas
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Cat# PVGS1487
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