Mouse CCL5 Recombinant Rat Monoclonal Antibody (HA601395)

UNIPROT #

P13501

PROTEIN NAME

Mouse CCL5

SYNONYMS

Beta chemokine RANTES antibody;Beta chemokine RANTES precursor antibody;C C motif chemokine 5 antibody;CCL 5 antibody;CCL5 antibody;CCL5_HUMAN antibody;Chemokine (C C motif) ligand 5 antibody;Chemokine CC Motif Ligand 5 antibody;D17S136E antibody;EoCP antibody;Eosinophil chemotactic cytokine antibody;MGC17164 antibody;RANTES(4-68) antibody;Regulated upon activation normally T expressed and presumably secreted antibody;SCYA 5 antibody;SCYA5 antibody;SIS delta antibody;SIS-delta antibody;SISd antibody;Small inducible cytokine A5 (RANTES) antibody;Small inducible cytokine A5 antibody;Small inducible cytokine subfamily A (Cys Cys) member 5 antibody;Small-inducible cytokine A5 antibody;T cell specific protein p288 antibody;T cell specific protein RANTES antibody;T cell specific RANTES protein antibody;T cell-specific protein P228 antibody;T-cell-specific protein RANTES antibody;TCP 228 antibody;TCP228 antibody

SUBCELLULAR LOCATION

Secreted.

FUNCTION

CCL5, also known as RANTES (Regulated upon Activation, Normal T cell Expressed and presumably Secreted), is an 8 kDa beta -chemokine that plays a primary role in the inflammatory immune response by means of its ability to attract and activate leukocytes. Human and mouse RANTES exhibit cross-species activity on human and mouse cells. 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. In humans, CCR5 binding to CCL5 inhibits the infectivity of R5 (M-tropic) but not X4 (T-tropic) strains of HIV-1. The two N-terminal residues of CCL5 can be removed by CD26/DPPIV, generating a protein that functions as a chemotaxis inhibitor and more effectively blocks M-tropic HIV-1 infection of monocytes. Oligomerization of CCL5 on glycosaminoglycans is required for CCR1-mediated 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 pro-inflammatory macrophages in addition to its actions on tumor cells, stromal cells, and the vasculature.