Recombinant Human CCL4 Protein, Mature chain, Tag Free, Biotinylated
Cat.No. : | CCL4-183H |
Product Overview : | Recombinant human MIP-1 beta (CCL4) protein was developed from E. coli. |
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Species : | Human |
Source : | E.coli |
Tag : | Non |
Protein Length : | 24-92 a.a. |
Description : | The protein encoded by this gene is a mitogen-inducible monokine and is one of the major HIV-suppressive factors produced by CD8+ T-cells. The encoded protein is secreted and has chemokinetic and inflammatory functions. |
Conjugation/Label : | Biotin |
Form : | Lyophilised |
Endotoxin : | Endotoxin level was found to be less than 0.1 ng/μg (1 EU/μg). |
Applications : | ELISA, WB |
Notes : | FOR RESEARCH USE ONLY (RUO). |
Storage : | The lyophilized protein is stable for at least 1 year from date of receipt at -20 centigrade. Upon reconstitution, this cytokine can be stored in working aliquots at -20 centigrade for six months, with a carrier protein without detectable loss |
Storage Buffer : | Lyophilised from 0.2 μm filtered PBS solution. |
Reconstitution : | Upon receipt a quick spin of the vial followed by reconstitution in distilled water to a concentration not less than 0.1 mg/mL. This solution can then be diluted into other buffers. |
Gene Name | CCL4 chemokine (C-C motif) ligand 4 [ Homo sapiens (human) ] |
Official Symbol | CCL4 |
Synonyms | CCL4; chemokine (C-C motif) ligand 4; LAG1, SCYA4, small inducible cytokine A4 (homologous to mouse Mip 1b); C-C motif chemokine 4; Act 2; AT744.1; MIP 1 beta; PAT 744; SIS-gamma; MIP-1-beta(1-69); CC chemokine ligand 4; secreted protein G-26; T-cell activation protein 2; small-inducible cytokine A4; lymphocyte-activation gene 1; G-26 T-lymphocyte-secreted protein; lymphocyte activation gene 1 protein; macrophage inflammatory protein 1-beta; small inducible cytokine A4 (homologous to mouse Mip-1b); ACT2; G-26; HC21; LAG1; LAG-1; MIP1B; SCYA2; SCYA4; MIP1B1; MIP-1-beta; MGC104418; MGC126025; MGC126026; |
Gene ID | 6351 |
mRNA Refseq | NM_002984 |
Protein Refseq | NP_002975 |
MIM | 182284 |
UniProt ID | P13236 |
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Case 1: Yang Y, et al. Int J Mol Med. 2017
Endothelial-mesenchymal transition (EndMT) is part of the atherosclerosis process. New research points out that foam cells from M1 macrophages boost EndMT by emitting more CCL-4. This extra CCL-4 makes the endothelial layers more porous and attracts more monocytes. Blocking CCL-4 reversed these effects since it acts through CCR-5 receptors and boosts TGF-β. Essentially, M1 foam cells increase EndMT via upregulated CCL-4, affecting permeability and monocyte adhesion.

Fig1. CCL-4 induces EndMT in a concentration- and time-dependent manner.

Fig2. Western blot analysis demonstrating the effect of CCL-4 at different concentration on the expression levels of VCAM-1 in HAECs.
Case 2: Deng H, et al. Cytokine. 2024
Osteoarthritis (OA) involves cartilage breakdown, and this study explored the role of CCL4 and CCR5 in that process. Researchers found that CCL4 levels rise in OA, which leads to more cell death and reactive oxygen species (ROS). CCL4 interacts with CCR5, kicking off the NF-κB signaling pathway. By using maraviroc, a CCR5 blocker, we saw decreased cartilage cell death, lower ROS, and less degradation.

Fig1. Western blot detection level in control group, CCL4 group, CCL4 + DMSO group and CCL4 + maraviroc group.

Fig2. Intracellular ROS levels detected by flow cytometry.

Fig1. Summary of vital role of CCL4 in aging-impaired vascular diseases. (Ting-Ting Chang, 2024)
Not For Human Consumption!
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