Interleukin 1 Receptor Like Protein 2 (IL1RL2) Antibody (Biotin)
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Description
IL1RL2 Antibody (Biotin) is a Rabbit Polyclonal against IL1RL2 conjugated to Biotin.
Documents del producto
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Interleukin 1 Receptor Like Protein 2 (IL1RL2) |
| Host | Rabbit |
| Reactivity | Human |
| Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Biotin |
| Isotype | IgG |
| Purity | > 95% |
| Purification | Purified by Protein G. |
| Size 1 | 20 µg |
| Size 2 | 50 µg |
| Size 3 | 100 µg |
| Size 4 | 200 µg |
| Size 5 | 1 mg |
| Form | Liquid |
| Tested Applications | ELISA |
| Buffer | 0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q9HB29 |
| Gene ID | 8808 |
| NCBI Accession | NP_003845.2, NM_003854.2 |
| OMIM | 604512 |
| Alias | IL1RL2, IL-1Rrp2, IL-36R, IL1R-rp2, IL1RRP2, IL-1R6 |
| Background | Antibody anti-IL1RL2 |
| Status | RUO |
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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