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A DNA sequence encoding the human MIP-1 alpha protein sequence (containing the signal peptide sequence, and the mature human MIP-1 alpha sequence) was expressed in modified human 293 cells.

Human Macrophage inflammatory protein-1alpha (MIP-1 alpha; MIP-1a) belongs to the chemokine family. Chemokines are small secreted molecules containing 4 conserved cysteine residues and 2 disulfide linkages. The first two cysteine residues of chemokine molecules may be in one of the following configurations, CC or CXC and this defines the two major chemokine sub-families. MIP-1 is a CC chemokine and its recent designation is chemokine ligand 3 (CCL3). MIP-1 alpha is constitutively expressed from platelets and bone marrow CD34 progenitor cells. MIP-1 alpha expression can also be induced by bacteria or bacterial products such as LPS in monocyte/macrophages, dendritic cells, neutrophils, microglial cells and in activated B and T cells. Expression of MIP-1 alpha has also been described in non-immune somatic cells such as fibroblasts, mucosal epithelial cells, osteoblasts and vascular smooth muscle cells. As a chemokine, MIP-1 alpha plays a role in the recruitment of leukocytes to the sites of infection, and is involved in the activation of cells and the inflammatory response. MIP-1 alpha is chemotactic for monocytes/macrophages, T cells, neutrophils, eosinophils, basophils, dendritic cells and NK cells. MIP-1 alpha also plays a role in the transendothelial migration of monocytes, T lymphocytes, neutrophils, and dendritic cells at sites of inflammation. MIP-1 alpha and MIP-1 beta is the major HIV-suppressive factors produced by CD8+ T-cells. Recombinant MIP-1 alpha has been shown to inhibit different strains of HIV-1, HIV-2, and simian immunodeficiency virus (SIV) in a dose-dependent manner. MIP-1 alpha is a peptide of 92 amino acids. MIP-1 alpha occurs naturally as a homodimer or a heterodimer with MIP-1 beta. For a review of MIP-1 alpha migration and signaling cascades please refer to Lentzsch S et al. (2003) Blood 101(9): 3568-73.