ATHB-52 Antibody
Description
PR Antibody (AB-52) - Progesterone Receptor Detection
Key Research Findings
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Detects nuclear progesterone receptors critical for reproductive biology
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Essential for studying hormone-responsive cancers (89% specificity in breast cancer studies)
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Recognizes both PR isoforms with equal affinity (KD = 2.3 nM)
Anti-Ro52/TRIM21 Antibodies - Autoimmune Disease Biomarker
Clinical Significance
| Disease Association | Prevalence | Odds Ratio |
|---|---|---|
| Sjögren's Syndrome | 58-72% | 4.1 |
| Systemic Lupus | 35-40% | 2.8 |
| Interstitial Lung Disease | 68% | 8.2 |
| Dermatomyositis | 43% | 3.1 |
Mechanistic Insights
Comparative Analysis of Antibody Targets
| Feature | AB-52 (PR) | Ro52 (TRIM21) |
|---|---|---|
| Molecular Weight | 120 kDa | 52 kDa |
| Cellular Localization | Nuclear | Cytoplasmic/Nuclear |
| Primary Function | Hormone receptor | Immune regulation |
| Disease Relevance | Cancer | Autoimmunity |
| Therapeutic Potential | Diagnostic marker | Treatment target |
Research Limitations & Opportunities
Product Specs
Target Background
Q&A
FAQs for Researchers on Anti-Ro52 Antibody (TRIM21)
What methodologies are recommended for detecting anti-Ro52 antibodies in autoimmune disease studies?
Methodological Answer:
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Detection Assays: Use enzyme-linked immunosorbent assay (ELISA) or line immunoblot assays for specificity. Commercial kits often detect anti-Ro52 alongside anti-Ro60/SSA and anti-La/SSB, but confirmatory testing with immunoprecipitation or cell-based assays is advised for validation .
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Co-Occurrence Analysis: Screen for concurrent autoantibodies (e.g., anti-ARS, anti-MDA5) using multiplex panels to assess overlap and clinical relevance .
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Clinical Correlation: Pair serological data with clinical parameters (e.g., interstitial lung disease [ILD], creatine kinase levels) to evaluate prognostic significance .
Table 1: Common Autoantibody Co-Occurrence in Anti-Ro52+ Patients (n=22)
How does anti-Ro52 positivity correlate with clinical outcomes in idiopathic inflammatory myopathies (IIM)?
Methodological Answer:
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Study Design: Retrospective cohort studies comparing anti-Ro52+ vs. anti-Ro52− IIM patients, focusing on ILD prevalence, glucocorticoid resistance, and mortality .
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Key Findings:
What experimental models elucidate the pathogenicity of anti-Ro52 antibodies in cardiac complications?
Methodological Answer:
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In Vivo Models: Immunize BALB/c mice with recombinant Ro52 protein to study congenital heart block (CHB). Monitor pups for ECG abnormalities (e.g., bradycardia, AV dissociation) .
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In Vitro Models: Apply anti-Ro52-positive sera to human embryonic kidney (HEK) cells expressing hERG potassium channels. Measure current reduction (IhERG) via patch clamp to link anti-Ro52 to long QT syndrome .
Key Data from Murine Studies
| Parameter | Anti-Ro52-Exposed Pups (n=20) | Control Pups (n=22) |
|---|---|---|
| Bradycardia | 20% (4/20) | 0% |
| Complete AV Block | 10% (2/20) | 0% |
| Mortality | 10% (2/20) | 0% |
| Source: |
How can researchers resolve contradictions in anti-Ro52’s association with interstitial lung disease (ILD)?
Methodological Answer:
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Cohort Stratification: Subgroup analysis by autoantibody clusters (e.g., anti-Ro52 with vs. without anti-ARS) to isolate ILD risk factors .
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Mechanistic Studies: Investigate Ro52’s role in interferon (IFN) signaling and viral response pathways using RNA sequencing of lung biopsies .
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Contradictory Data Example: While anti-Ro52 correlates with ILD in PM/DM , systemic sclerosis (SSc) cohorts show no significant association .
Table 2: Confounding Factors in ILD Studies
| Factor | PM/DM Cohort | SSc Cohort |
|---|---|---|
| Anti-Ro52 Prevalence | 55.0% | 10–30% |
| ILD Linkage Mechanism | IFN pathway activation | Myositis-independent |
| Survival Impact | Reduced | Neutral |
What novel research directions address anti-Ro52’s role in B-cell activation and autoimmunity?
Methodological Answer:
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Single-Cell Sequencing: Profile B-cell receptors in anti-Ro52+ patients to identify clonal expansions (e.g., IGHV3-23 usage) .
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Functional Studies: Knockout TRIM21 in murine models to assess its role in IgG clearance and innate immunity .
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Therapeutic Targets: Explore small-molecule inhibitors of Ro52’s E3 ubiquitin ligase activity to modulate IFN responses .
