CCL4 (MIP-1 beta) Mouse anti-Human, PerCP-eFluor 710, Clone: FL34Z3L, eBioscience™

Mouse Monoclonal Antibody

Brand: Affymetrix eBioscience

Manufacturer Part Number: 46-7540-41

25TEST Anti-Human CCL4 (MIP-1 beta) PerCP-eFluor 710

Code: NEW

Additional Details:
Additional Details: Weight: 0.23750kg

Disclaimers: For Research Use Only.

Product Code. 15579366

Quantity Price
1 £114.70 / 25 tests
Estimated Shipment date
from Supplier 25-10-2016
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Description and Specification


Antigen CCL4 (MIP-1 beta)
Applications Flow Cytometry
Applications Flow Cytometry (Intracellular Staining)
Clone FL34Z3L
Concentration 5μL (0.03μg)/test
Conjugate PerCP-eFluor 710
Format Conjugated
Formulation aqueous buffer, 0.09% sodium azide, may contain carrier protein/stabilizer
Gene Alias C-C Motif Chemokine 4, Macrophage Inflammatory Protein 1 beta
Host Species Mouse
Isotype IgG2a
Quantity 25 tests
Regulatory Status RUO
Species Reactivity Human
Storage Requirements Store at 2-8°C. Do not freeze. Light-sensitive material.
Primary or Secondary Primary
Monoclonal or Polyclonal Monoclonal

This FL34Z3L monoclonal antibody reacts with human CCL4. CCL4, also known as MIP-1 beta (Macrophage Inflammatory Protein 1 beta), 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. While both CCL3 and CCL4 are chemoattractant for monocytes, macrophages, and dendritic cells, CCL4 preferentially attracts CD4+ T cells, while CD8+ T cells are more responsive to CCL3. 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.