Code | CSB-EP004775HU |
Abbreviation | Recombinant Human CCL11 protein |
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Size | $224 |
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To produce recombinant human Eotaxin (CCL11) in E. coli, the gene encoding the full-length CCL11 protein (1-97aa) is co-cloned into an expression vector with an N-terminal GST-tag gene and transformed into E. coli cells. The bacteria are grown under conditions that induce protein expression. After sufficient growth, the cells are lysed to release the recombinant CCL11 protein. Purification of this recombinant CCL11 protein is conducted by affinity chromatography. Its purity is measured using SDS-PAGE, exceeding 90%.
Human CCL11 is expressed by primary human fibroblasts and is crucial for eosinophilic chemotaxis [1]. Studies have shown that CCL11 is overexpressed in human atopic dermatitis (AD) and can be upregulated by perturbating the Ikkb-NF-κB pathway in human dermal fibroblasts [2]. CCL11 can induce angiogenic responses via the CCR3 receptor expressed by human microvascular endothelial cells [3].
CCL11 has been implicated in various immune responses. It can increase the proportion of regulatory T cells (Tregs) and the production of IL-2 and TGF-β by CD4+ T cells through the STAT5 signaling pathway [4]. Increased production of CCL11 is associated with aging and neuropsychiatric disorders [5]. Additionally, CCL11 levels are linked to long-term functional outcomes in patients following ischemic stroke [6].
Furthermore, CCL11 modulates monolayer permeability in human coronary artery endothelial cells and can enhance eosinophil chemotactic activity in asthma [7][8]. CCL11 expression in human airway smooth muscle cells is mediated by IL-17A through the STAT3 pathway [9].
References:
[1] X. Zhou, H. Hu, S. Balzar, J. Trudeau, & S. Wenzel, Mapk regulation of il-4/il-13 receptors contributes to the synergistic increase in ccl11/eotaxin-1 in response to tgf-β1 and il-13 in human airway fibroblasts, The Journal of Immunology, vol. 188, no. 12, p. 6046-6054, 2012. https://doi.org/10.4049/jimmunol.1102760
[2] K. Ko, J. Merlet, B. DerGarabedian, Z. Huang, Y. Suzuki-Horiuchi, M. Hedberget al., Nf-κb perturbation reveals unique immunomodulatory functions in prx1+ fibroblasts that promote development of atopic dermatitis, Science Translational Medicine, vol. 14, no. 630, 2022. https://doi.org/10.1126/scitranslmed.abj0324
[3] R. Salcedo, H. Young, M. Ponce, J. Ward, H. Kleinman, W. Murphyet al., Eotaxin (ccl11) induces in vivo angiogenic responses by human ccr3+ endothelial cells, The Journal of Immunology, vol. 166, no. 12, p. 7571-7578, 2001. https://doi.org/10.4049/jimmunol.166.12.7571
[4] R. Wang and K. Huang, Ccl11 increases the proportion of cd4+cd25+foxp3+ treg cells and the production of il‑2 and tgf‑β by cd4+ t�cells via the stat5 signaling pathway, Molecular Medicine Reports, 2020. https://doi.org/10.3892/mmr.2020.11049
[5] M. Ivanovska, Z. Abdi, M. Murdjeva, D. Macêdo, A. Maes, & M. Maes, Ccl11 or eotaxin-1: an immune marker for ageing and accelerated ageing in neuro-psychiatric disorders,, 2020. https://doi.org/10.20944/preprints202001.0370.v1
[6] M. Roy-O’Reilly, R. Ritzel, S. Conway, I. Staff, G. Fortunato, & L. McCullough, Ccl11 (eotaxin-1) levels predict long-term functional outcomes in patients following ischemic stroke, Translational Stroke Research, vol. 8, no. 6, p. 578-584, 2017. https://doi.org/10.1007/s12975-017-0545-3
[7] M. Jamaluddin, X. Wang, H. Wang, C. Rafael, Q. Yao, & C. Chen, Eotaxin increases monolayer permeability of human coronary artery endothelial cells, Arteriosclerosis Thrombosis and Vascular Biology, vol. 29, no. 12, p. 2146-2152, 2009. https://doi.org/10.1161/atvbaha.109.194134
[8] G. Dent, C. Hadjicharalambous, T. Yoshikawa, R. Handy, J. Powell, I. Andersonet al., Contribution of eotaxin-1 to eosinophil chemotactic activity of moderate and severe asthmatic sputum, American Journal of Respiratory and Critical Care Medicine, vol. 169, no. 10, p. 1110-1117, 2004. https://doi.org/10.1164/rccm.200306-855oc
[9] A. Saleh, L. Shan, A. Halayko, S. Kung, & A. Gounni, Critical role for stat3 in il-17a-mediated ccl11 expression in human airway smooth muscle cells, The Journal of Immunology, vol. 182, no. 6, p. 3357-3365, 2009. https://doi.org/10.4049/jimmunol.0801882
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