Phospho-RIPK2 (Ser176) Antibody

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Description

Introduction

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 .

Key Features

CharacteristicDetails
TargetRIPK2 (phosphorylated at Ser176)
ImmunogenSynthetic peptide derived from human RIPK2 (AA 146–195)
Host SpeciesRabbit
ClonalityPolyclonal
ConjugateUnconjugated
ReactivityHuman, Mouse
PurificationAffinity chromatography using phospho peptide
FormulationLiquid in PBS with glycerol and sodium azide
ApplicationsWestern blotting (WB), Immunohistochemistry (IHC), ELISA, Immunofluorescence (IF)

Applications and Dilution Ranges

The antibody is validated for multiple research techniques, with recommended dilutions as follows :

MethodDilution Range
Western Blotting1:500–1:2000
Immunohistochemistry1:100–1:300
ELISA1:10,000–1:40,000
Immunofluorescence1:50–1:200

Role in Immune Signaling

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 .

Disease Implications

  • 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 .

Mechanistic Insights

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 .

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