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Cat.No.: F3023
| Dilution |
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|
| Application |
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| WB, IP, IF, FCM |
| Reactivity |
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| Mouse |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 24 kDa |
| Positive Control | Raw 264.7 cells (LPS, 100 ng/ml, 6 h) |
|---|---|
| Negative Control | Raw 264.7 cells |
| Specificity |
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| IL-6 Antibody [F4K18] detects endogenous levels of total IL-6 protein. |
| Clone |
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| F4K18 |
| Synonym(s) |
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| Interleukin-6; IL-6; B-cell stimulatory factor 2 (BSF-2); CTL differentiation factor (CDF); Hybridoma growth factor; Interferon beta-2 (IFN-beta-2); IL6; IFNB2 |
| Background |
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| Interleukin-6 (IL-6), a pleiotropic glycoprotein cytokine with a four-helix bundle structure and a conserved disulfide bond between Cys44 and Cys50, serves as a central mediator of acute phase responses and immune regulation by binding its α-receptor (IL-6R) to form a high-affinity complex with gp130, which then triggers JAK1/JAK2-mediated tyrosine phosphorylation of gp130 and recruits STAT3 (Tyr705) for nuclear translocation and transcriptional activation of target genes. IL-6 possesses site I/II/III interfaces where key residues such as Phe171, Arg167, and Pro33 mediate receptor docking, with classic signaling via membrane-bound IL-6R driving anti-inflammatory and hepatocyte effects (such as C-reactive protein and fibrinogen induction), while trans-signaling through soluble IL-6R promotes pro-inflammatory responses via activation of MAPK/ERK, PI3K/Akt, and SHP2 pathways. IL-6 stimulates hepatic acute phase protein synthesis, drives B-cell differentiation into plasma cells with IgM and IgG production, induces Th17 polarization while inhibiting Treg differentiation, and coordinates monocyte-to-macrophage transition during infection and injury. IL-6 balances innate and adaptive immunity as well as hematopoiesis, while pathologically, chronic elevation leads to rheumatoid arthritis with synovial inflammation and joint destruction via RANKL-mediated osteoclastogenesis, supports plasma cell survival and proliferation in multiple myeloma, and contributes to cancer cachexia through STAT3-mediated metabolic reprogramming. |
| References |
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