The CCR5 and the CCL5 ligand have been detected in some hematological malignancies, lymphomas, and a great number of solid tumors, but extensive studies on the role of the CCL5 CCR axis were performed only in a limited number of cancers. CCL5 Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with N-hFc tag. The predicted molecular weight is 35.2 kDa and the accession number is P30882.
The CCR5 and the CCL5 ligand have been detected in some hematological malignancies, lymphomas, and a great number of solid tumors, but extensive studies on the role of the CCL5 CCR axis were performed only in a limited number of cancers. CCL5 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in E. coli expression system with N-His-Avi tag. The predicted molecular weight is 10.89 kDa and the accession number is P13501.
CCL5 Protein, Human, Recombinant is expressed in E. coli expression system. The predicted molecular weight is 8 kDa and the accession number is D0EI67.
CCL5 Protein, Human, Recombinant (His & mucin) is expressed in HEK293 mammalian cells with His and mucin tag. The predicted molecular weight is 34 kDa and the accession number is D0EI67.
C-C motif chemokine 5(CCL5) is a β-chemokine that plays a primary role in the inflammatory immune response by means of its ability to attract and activate leukocytes. CCL5 is secreted by many cell types at inflammatory sites, and it exerts a wide range of activities through the receptors CCR1, CCR3, CCR4, and CCR5. Inflammatory responses can be impaired by the sequestration of CCL5 by the cytomegalovirus protein US28. Oligomerization of CCL5 on glycosaminoglycans is required for CCR1mediated leukocyte adhesion and activation as well as CCL5’s interaction with the chemokine CXCL4 PF4.The deposition of CCL5 on activated vascular endothelial cells is crucial for monocyte adhesion to damaged vasculature, but CCL5 oligomerization is not required for the extravasation of adherent leukocytes.CCL5 is upregulated in breast cancer and promotes tumor progression through the attraction of proinflammatory macrophages in addition to its actions on tumor cells, stromal cells, and the vasculature.
Ccl12 prevented initiation of the reparative response by prolonging inflammation and inhibiting fibroblast conversion to myofibroblasts, resulting in diminished scar formation. Macrophage secretion of Ccl12 directly impaired fibronectin and collagen deposition and indirectly stimulated collagen degradation through upregulation of matrix metalloproteinase-2. In post-MI patients, circulating LPS levels strongly associated with the Ccl12 homologue monocyte chemotactic protein 1 (MCP-1). Both MCP-1 and MCP-5 are HIF-1 target genes and that HIF-1alpha is involved in transcriptional induction of these two chemokines in astrocytes by hypoxia.