Code | CSB-AP000821HU |
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Size | $142 |
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The Recombinant Human CCL2 protein is a vital research tool for investigators in the field of immunology. This C-C motif chemokine 2, also referred to as CCL2, MCP1, and SCYA2, is produced in E. coli and spans the 24-99aa expression region, representing the full-length mature protein. The tag-free protein is provided as a lyophilized powder, facilitating straightforward reconstitution using sterile water or a suitable buffer to cater to diverse experimental requirements.
Our Recombinant Human CCL2 protein showcases a high level of purity, surpassing 96%, as confirmed by both SDS-PAGE and HPLC assessments. Endotoxin levels are stringently controlled to remain below 1.0 EU/µg, as verified using the LAL method. This protein is fully biologically active, as illustrated by its effectiveness in a chemotaxis bioassay with human monocytes, exhibiting a functional concentration range of 10-100 ng/ml.
The CCL2 chemokine has been widely studied in scientific research. Matsushima and Oppenheim (1989)[1] first reported the identification and purification of the monocyte chemotactic and activating factor, later known as CCL2. In 2013, Deshmane et al.[2] provided a comprehensive review of the multifaceted roles of CCL2 in inflammation and disease pathogenesis, including its implications in cancer progression. More recently, Yang et al. (2018)[3] highlighted the potential use of CCL2 as a diagnostic biomarker for rheumatoid arthritis. These studies emphasize the significance of CCL2 in immune system function and suggest its possible therapeutic value in treating various immune-related diseases.
References:
1. Matsushima K, Oppenheim JJ. Interleukin 8 and MCAF: novel inflammatory cytokines inducible by IL 1 and TNF. Cytokine. 1989;1(1):2-13.
2. Deshmane SL, et al. Monocyte Chemoattractant Protein-1 (MCP-1): An Overview. J Interferon Cytokine Res. 2009;29(6):313-26.
3. Yang M, et al. The diagnostic value of serum CCL2/MCP-1 levels in patients with rheumatoid arthritis. Ann Palliat Med. 2018;7(3):312-8.
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