|Application ||WB, IHC|
|Calculated MW||10212 Da|
|Positive Control||Western blot: Mouse Bladder tissue lysate, IHC: human prostate carcinoma|
|Application & Usage||Western blot: ~1:1000, IHC: ~1:10–1:50.|
|Other Names||CCL4; LAG1; MIP1B; SCYA4; C-C motif chemokine 4; G-26 T-lymphocyte-secreted protein; HC21; Lymphocyte activation gene 1 protein; MIP-1-beta(1-69); Macrophage inflammatory protein 1-beta; PAT 744; Protein H400; SIS-gamma; Small-inducible cytokine A4; T-cell activation protein 2.|
|Formulation||100 µl of antibody in PBS with 0.09% (W/V) sodium azide|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||CCL4 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||LAG1, MIP1B, SCYA4|
|Function||Monokine with inflammatory and chemokinetic properties. Binds to CCR5. One of the major HIV-suppressive factors produced by CD8+ T-cells. Recombinant MIP-1-beta induces a dose-dependent inhibition of different strains of HIV-1, HIV-2, and simian immunodeficiency virus (SIV). The processed form MIP-1-beta(3-69) retains the abilities to induce down-modulation of surface expression of the chemokine receptor CCR5 and to inhibit the CCR5- mediated entry of HIV-1 in T-cells. MIP-1-beta(3-69) is also a ligand for CCR1 and CCR2 isoform B.|
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Provided below are standard protocols that you may find useful for product applications.
CCL4 is a member of the CC- subfamily of chemokines and is most closely related to CCL3, or MIP-1 alpha. These proteins play critical roles in the recruitment of leukocytes to the site of inflammation. In addition to its chemotactic functions, CCL4 induces the release of proinflammatory cytokine, mast cells degranulation, and NK cell activation. CCL4 signaling is mediated by the G protein-coupled receptors CCR1, CCR4, and CCR5, which are shared with CCL3 and CCL5 (RANTES). CCR5 is the primary co-receptor for HIV entry, which the virus binds through the gp120 envelope protein. All CCR5 ligands demonstrate potent inhibition of virus entry into the cell, both through steric hindrance of gp120-CCR5 interaction, and ligand-mediated receptor internalization.
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