| Expression System | CHO |
| Aggregation | < 5% as determined by SEC-HPLC |
| Purity | > 95% as determined by SDS-PAGE |
| Sterility | 0.22 μm Filtered |
| Clone | PRO2198 |
| Source/Isotype | Human IgG4 (S228P),Kappa |
| Application | Bioactivity-ELISA |
| Specificity | Detects IL-4R、IL31 |
| Gene | IL-4R&IL31 |
| Other Names | IL-4R：CD124,IL4RA IL31：IL-31, IL31, Interleukin-31 |
| Gene ID | IL-4R：3566 (human) IL31：86653 (human) |
| Background | The genetic research background of IL-4R versus IL-31 stems from its central pathological role in Th2-type immune diseases such as atopic dermatitis: IL-4R α as a key mediator of IL-4 and Il-13 signaling pathways, IL-4R α as a key mediator of IL-4 and Il-13 signaling pathways, IL-4R as a key mediator of Il-13 signaling, and IL-3R as a key mediator of Il-13 signaling, by activating downstream cascades such as Jak/STAT, which drive inflammatory factor release with skin barrier dysfunction; whereas Il-31 is secreted by activated Th2 cells, by binding to its receptor IL-31RA/OSMR β complex, IL-31RA/OSMR β is released by activated Th2 cells, direct activation of sensory neurons cause severe itching, the formation of“Inflammation-itching-scratching” vicious cycle. The sustained activation of il-4rα can induce the expression of IL-31, and then amplify the immune inflammatory response. |
| Formulation | Phosphate-buffered solution, pH 7.2-7.4. |
| Endotoxin | < 1 EU/mg, determined by LAL gel clotting assay |
| Expression System | CHO |
| Aggregation | < 5% as determined by SEC-HPLC |
| Purity | > 95% as determined by SDS-PAGE |
| Sterility | 0.22 μm Filtered |
| Clone | PRO2198 |
| Source/Isotype | Human IgG4 (S228P),Kappa |
| Application | Bioactivity-ELISA |
| Specificity | Detects IL-4R、IL31 |
| Gene | IL-4R&IL31 |
| Other Names | IL-4R：CD124,IL4RA IL31：IL-31, IL31, Interleukin-31 |
| Gene ID | IL-4R：3566 (human) IL31：86653 (human) |
| Background | The genetic research background of IL-4R versus IL-31 stems from its central pathological role in Th2-type immune diseases such as atopic dermatitis: IL-4R α as a key mediator of IL-4 and Il-13 signaling pathways, IL-4R α as a key mediator of IL-4 and Il-13 signaling pathways, IL-4R as a key mediator of Il-13 signaling, and IL-3R as a key mediator of Il-13 signaling, by activating downstream cascades such as Jak/STAT, which drive inflammatory factor release with skin barrier dysfunction; whereas Il-31 is secreted by activated Th2 cells, by binding to its receptor IL-31RA/OSMR β complex, IL-31RA/OSMR β is released by activated Th2 cells, direct activation of sensory neurons cause severe itching, the formation of“Inflammation-itching-scratching” vicious cycle. The sustained activation of il-4rα can induce the expression of IL-31, and then amplify the immune inflammatory response. |
| Formulation | Phosphate-buffered solution, pH 7.2-7.4. |
| Endotoxin | < 1 EU/mg, determined by LAL gel clotting assay |
