The Phospho-RIPK2 (Ser176) Antibody is a highly specific rabbit polyclonal antibody designed to detect endogenous levels of Receptor-Interacting Serine-Threonine Kinase 2 (RIPK2) protein only when phosphorylated at Serine 176 (S176). This antibody is widely used in molecular biology and immunology research to study RIPK2 activation in signaling pathways, particularly in immune responses and inflammatory processes .
| Characteristic | Details |
|---|---|
| Target | RIPK2 (phosphorylated at Ser176) |
| Immunogen | Synthetic peptide derived from human RIPK2 (AA 146–195) |
| Host Species | Rabbit |
| Clonality | Polyclonal |
| Conjugate | Unconjugated |
| Reactivity | Human, Mouse |
| Purification | Affinity chromatography using phospho peptide |
| Formulation | Liquid in PBS with glycerol and sodium azide |
| Applications | Western blotting (WB), Immunohistochemistry (IHC), ELISA, Immunofluorescence (IF) |
The antibody is validated for multiple research techniques, with recommended dilutions as follows :
| Method | Dilution Range |
|---|---|
| Western Blotting | 1:500–1:2000 |
| Immunohistochemistry | 1:100–1:300 |
| ELISA | 1:10,000–1:40,000 |
| Immunofluorescence | 1:50–1:200 |
RIPK2 phosphorylation at S176 is critical for its activation in innate immune pathways. Studies using this antibody have shown that phosphorylation at S176 enhances RIPK2 kinase activity, enabling downstream signaling through NF-κB and MAPK pathways . For example, in osteoarthritis models, MYSM1-mediated dephosphorylation of RIPK2 at S176 reduces NF-κB activation, thereby mitigating inflammation .
Osteoarthritis: Overexpression of MYSM1 reduces RIPK2 S176 phosphorylation, suppressing chondrocyte degeneration .
Inflammatory Disorders: RIPK2 S176 phosphorylation correlates with ubiquitination and activation of pro-inflammatory pathways, making it a therapeutic target in diseases like Crohn’s and rheumatoid arthritis .
Phosphorylation at S176 promotes RIPK2 ubiquitination (e.g., 'Lys-63' and 'Met-1' linked chains), which recruits downstream effectors like IKBKG/NEMO and TAB2/TAB3 . This antibody has been instrumental in demonstrating that sustained S176 phosphorylation (e.g., via RIPK2 S176D mutation) enhances NF-κB and MAPK activation, even in the presence of MYSM1 .