Mouse Soluble interleukin 6 Receptor ELISA Kit (RMEK-0153945)
Cat. No.: RMEK-0153945
Category: ELISA Kits
INQUIRY
1 x 96 tests
This ELISA kit is a 1. 5 hour solid-phase ELISA designed for the quantitative determination of the targets. This ELISA kit for research use only, not for therapeutic or diagnostic applications!
Product Features
| Species Reactivity | Mouse |
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| Assay Time | 1.5 h |
Target Information
| Target Symbol | Sil 6R/cd126 |
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| UniProt ID | P08887 |
| Function | Part of the receptor for interleukin 6. Binds to IL6 with low affinity, but does not transduce a signal. Signal activation necessitate an association with IL6ST. Activation leads to the regulation of the immune response, acute-phase reactions and hematopoiesis. The interaction with membrane-bound IL6R and IL6ST stimulates 'classic signaling', the restricted expression of the IL6R limits classic IL6 signaling to only a few tissues such as the liver and some cells of the immune system. Whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells (Probable). [Isoform 1]: Signaling via the membrane-bound IL6R is mostly regenerative and anti-inflammatory (Probable). Drives naive CD4(+) T cells to the Th17 lineage, through 'cluster signaling' by dendritic cells (By similarity). [Isoform 2]: Soluble form of IL6 receptor (sIL6R) that acts as an agonist of IL6 activity. The IL6:sIL6R complex (hyper-IL6) binds to IL6ST/gp130 on cell surfaces and induces signaling also on cells that do not express membrane-bound IL6R in a process called IL6 'trans-signaling'. sIL6R is causative for the pro-inflammatory properties of IL6 and an important player in the development of chronic inflammatory diseases. In complex with IL6, is required for induction of VEGF production. Plays a protective role during liver injury, being required for maintenance of tissue regeneration (By similarity). 'Trans-signaling' in central nervous system regulates energy and glucose homeostasis (By similarity). [Soluble interleukin-6 receptor subunit alpha]: Soluble form of IL6 receptor (sIL6R) that acts as an agonist of IL6 activity. The IL6:sIL6R complex (hyper-IL6) binds to IL6ST/gp130 on cell surfaces and induces signaling also on cells that do not express membrane-bound IL6R in a process called IL6 'trans-signaling'. sIL6R is causative for the pro-inflammatory properties of IL6 and an important player in the development of chronic inflammatory diseases. In complex with IL6, is required for induction of VEGF production. Plays a protective role during liver injury, being required for maintenance of tissue regeneration (By similarity). 'Trans-signaling' in central nervous system regulates energy and glucose homeostasis (By similarity). |
| Cellular Localization | [Isoform 1]: Cell membrane; Single-pass type I membrane protein. [Isoform 2]: Secreted. [Soluble interleukin-6 receptor subunit alpha]: Secreted. |
| Domain | The two fibronectin type-III-like domains, contained in the N-terminal part, form together a cytokine-binding domain. The WSXWS motif appears to be necessary for proper protein folding and thereby efficient intracellular transport and cell-surface receptor binding. |
| Post-transcriptional Modifications | A short soluble form is released from the membrane by proteolysis. The sIL6R is formed mostly by limited proteolysis of membrane-bound receptors, a process referred to as ectodomain shedding, but is also directly secreted from the cells after alternative mRNA splicing. mIL6R is cleaved by the proteases ADAM10 and ADAM17. Glycosylated. Glycosylation is dispensable for transport, signaling, and cell-surface turnover. Glycosylation at Asn-55 is a protease-regulatory exosite. Glycosylation is required for ADAM17-mediated proteolysis. |
| Involvement in Disease | Hyper-IgE recurrent infection syndrome 5, autosomal recessive (HIES5): An immunologic disorder characterized by recurrent sinopulmonary and deep skin infections, mostly caused by bacteria, including H. influenza and Staphylococcus aureus. Additional features include asthma, atopic dermatitis, and impaired inflammatory responses during infection. Disease onset is in early infancy. The disease is caused by variants affecting the gene represented in this entry. |
Storage & Shipping
| Storage | Store at 2-8°C |
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| Shipping | Gel Packs |
| Stability | The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. |
For research use only. Not for clinical use.
