NAA Services for Anti-Lipoprotein-related Protein Receptor 4 (LRP4)

Creative Biolabs is an undisputed global leader in the custom natural autoantibody (NAA) analysis and provides comprehensive NAA services for various biomarkers for a wide variety of diseases. Our high-quality services will contribute greatly to the success of your project and they can be used as a specific biomarker to be applied to disease-specific autoantibodies tests. Here, we offer high-quality anti-lipoprotein-related protein receptor 4 (LRP4) autoantibody service for disease diagnosis and treatment.

Background of Anti-lipoprotein-related Protein Receptor 4 (LRP4) Antibody

LRP4, a member of the low-density lipoprotein receptor (LDLR) family, contains an enormously large extracellular N-terminal region that possesses multiple EGF repeats and LDLR repeats, a transmembrane domain, and a short C-terminal region. It is a receptor of agrin critical for acetylcholine receptor (AChR) clustering, muscle-specific tyrosine kinase (MuSK) activation, and neuromuscular junction (NMJ) formation. Anti-LRP4 autoantibodies are pathogenic in causing myasthenia gravis (MG), uncovered underlying pathological mechanisms, and revealed an important role of LRP4 in NMJ maintenance in adulthood. Autoantibodies to LRP4 inhibit binding of LRP4 to its ligand and predominantly belong to the immunoglobulin G1 (IgG1) subclass, which fixes complement, and thus may damage the postsynaptic muscle membrane by a similar mechanism as those to the AChR.

Fig.1 Reduced signal transmission in the NMJ induced by anti-LRP4 auto-antibodies. (Golfinopoulou, et al., 2023)Fig.1 Auto-antibodies against LRP4 in the NMJ.1

The Role of Anti-LRP4 Antibody in Myasthenia Gravis (MG)

MG is the most common disorder affecting the NMJ. In autoimmune MG, the identification of antibodies and characterization of serological subgroups is of great importance for diagnosis and management of the disease. MG is frequently caused by autoantibodies against AChR and MuSK. However, a proportion of MG patients are double-negative for anti-AChR and anti-MuSK antibodies. Recent studies in these subjects have identified autoantibodies against low-density LRP4. LRP4 autoantibodies were detected in 2%-45% of double-seronegative MG patients that lack antibodies against AChR and MuSK in different ethnicities and countries of origin. These results suggest that double-seronegative MG may be an autoimmune disorder caused by antibodies against LRP4. It is recommended that testing for anti-LRP4 antibodies should be considered when the clinical suspicion for MG is high despite negative conventional diagnostic tests.

Schematic of the NMJ and the main molecules involved in congenital myasthenic syndromes.Fig.2 Schematic of the NMJ and the main molecules involved in congenital myasthenic syndromes. (Rodríguez Cruz, 2018)

What We Can Do about NAA?

Equipped with our well-established platforms and experienced scientists, we can provide comprehensive autoantibody analysis services, from NAA detection, NAA profiling, to NAA epitope mapping. A wide spectrum of NAA products is available for your choice.

Features of Our Services

Academic findings indicate that monitoring the titer of anti-LRP4 antibody can be useful for assessing disease activity as well as decision making during treatment. Based on years of extensive experience in disease diagnosis and NAA analysis, Creative Biolabs can offer a full range of high-quality autoantibody services against LRP4 biomarker for diagnosis of MG. With the help of our professional scientists, we are confident in providing unique services to meet every customer's requirements. We can also provide custom services to meet the specific demand. Please feel free to contact us for more information.

References

  1. Golfinopoulou, Rebecca, et al. "Delving into Molecular Pathways: Analyzing the Mechanisms of Action of Monoclonal Antibodies Integrated in IMGT/mAb-DB for Myasthenia Gravis." Vaccines 11.12 (2023): 1756.
  2. Rodríguez Cruz, Pedro M., Jacqueline Palace, and David Beeson. "The neuromuscular junction and wide heterogeneity of congenital myasthenic syndromes." International journal of molecular sciences 19.6 (2018): 1677.
For Research Use Only | Not For Clinical Use

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