Human Interleukin 1 Receptor Like Protein 2 (IL1RL2) Protein (Active)
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Description
Human IL-1 Receptor-Like 2 Protein is a recombinant protein from Human produced in Human Cells. Recombinant Human Interleukin-1 receptor-like 2 is produced by our Mammalian expression system and the target gene encoding Asp20-Tyr337 is expressed with a Fc tag at the C-terminus.
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Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | IL-1 Receptor-Like 2 |
| Host | Human |
| Origin | Human |
| Observed MW | Molecular Weight: 63.1 kDa Sequence Fragment: Asp20-Tyr337 Tag: C-terminal Fc tag |
| Expression | Recombinant |
| Purity | > 95% (SDS-PAGE) |
| Size 1 | 10 µg |
| Size 2 | 50 µg |
| Form | Lyophilized |
| Tested Applications | SDS-PAGE |
| Buffer | PBS, pH7.4. |
| Availability | Shipped within 5-15 working days. |
| Storage | Store at < -20°C. |
| Dry Ice | No |
| UniProt ID | Q9HB29 |
| Alias | IL1RL2, IL-1Rrp2, IL-36R, IL1R-rp2, IL1RRP2, IL-1R6 |
| Background | Protein IL1RL2 |
| Status | RUO |
| Note | This product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use. |
Descripción
IL1RL2, also known as IL-36 receptor, is a key component of the interleukin-1 receptor (IL-1R) family, mediating IL-36 cytokine signaling to regulate inflammatory and immune responses. IL1RL2 forms a heterodimeric complex with the IL-1 receptor accessory protein (IL1RAP) upon IL-36 ligand binding, leading to the recruitment of MyD88, which activates downstream NF-κB, MAPK, and JNK signaling pathways. These pathways promote the production of pro-inflammatory cytokines and chemokines such as IL-6, TNF-α, and CXCL1, driving immune cell activation and tissue inflammation. IL1RL2 is predominantly expressed in epithelial cells, immune cells, and tissues like the skin and lungs, where it plays essential roles in host defense against infections and the regulation of inflammation. Dysregulation of IL1RL2 has been implicated in inflammatory diseases such as psoriasis, inflammatory bowel disease, and rheumatoid arthritis, where excessive IL-36 signaling exacerbates tissue damage and chronic inflammation. Knockdown studies reveal impaired IL-36 signaling, reduced cytokine production, and decreased immune activation, highlighting its critical role in inflammation, epithelial immunity, and disease pathogenesis.
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