ArticleJournal of immunological methods2011
MAp19, the alternative splice product of the MASP2 gene.
Article in Journal of immunological methods, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 70 citations in OpenAlex.
- Trial
- Investigations on collectin liver 1.The Journal of biological chemistry · 2013Trial
- Thrombomodulin Shapes Thrombo-Inflammatory Interactions in Lupus Nephritis.Scandinavian journal of immunology · 2026Article
- Research progress on the lectin pathway of complement in IgA nephropathy.Frontiers in immunology · 2026Review
- Complement proteins in axial spondyloarthritis: associations with disease activity and TNFi treatment response in a multicentre RCT.Rheumatology advances in practice · 2025Article
- The Complement System.Advances in experimental medicine and biology · 2025Review
- Complement activation in immunological neurological disorders: mechanisms and therapeutic strategies.Frontiers in neurology · 2025Review
- Article
- Complement and COVID-19: Three years on, what we know, what we don't know, and what we ought to know.Immunobiology · 2023Review
- Platelets and the Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus or Antiphospholipid Syndrome.TH open : companion journal to thrombosis and haemostasis · 2023Article
- Tinker, tailor, soldier, cell: the role of C-type lectins in the defense and promotion of disease.Protein & cell · 2023Review
- Mannan-binding lectin serine protease-2 (MASP-2) in human kidney and its relevance for proteolytic activation of the epithelial sodium channel.Scientific reports · 2022Article
- Low levels of the innate immune system proteins MASP-2 and MAp44 in patients with common variable immunodeficiency.Scandinavian journal of immunology · 2022Article
- The Contribution of Complement to the Pathogenesis of IgA Nephropathy: Are Complement-Targeted Therapies Moving from Rare Disorders to More Common Diseases?Journal of clinical medicine · 2021Review
- Review
- Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens.Frontiers in physics · 2021Article
- Review
- MAp34 Regulates the Non-specific Cell Immunity of Monocytes/Macrophages and Inhibits the Lectin Pathway of Complement Activation in a Teleost Fish.Frontiers in immunology · 2020Article
- Classical and lectin complement pathways and markers of inflammation for investigation of susceptibility to infections among healthy older adults.Immunity & ageing : I & A · 2020Article
- Remote ischemic preconditioning does not influence lectin pathway protein levels in head and neck cancer patients undergoing surgery.PloS one · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lectin pathway of complement is a central part of innate immunity, but as a powerful inducer of inflammation it needs to be tightly controlled. The MASP2 gene encodes two proteins, MASP-2 and MAp19. MASP-2 is the serine protease responsible for lectin pathway activation. The smaller alternative splice product, MAp19, lacks a catalytic domain but retains two of three domains involved in association with the pattern-recognition molecules (PRMs): mannan-binding lectin (MBL), H-ficolin, L-ficolin and M-ficolin. MAp19 reportedly acts as a competitive inhibitor of MASP-2-mediated complement activation. In light of a ten times lower affinity of MAp19, versus MASP-2, for association with the PRMs, much higher serum concentrations of MAp19 than MASP-2 would be required for MAp19 to exert such an inhibitory activity. Just four amino acid residues distinguish MAp19 from MASP-2, and these are conserved between man, mouse and rat. Nonetheless we generated monoclonal rat anti-MAp19 antibodies and established a quantitative assay. We found the concentration of MAp19 in serum to be 217 ng/ml, i.e., 11nM, comparable to the 7 nM of MASP-2. In serum all MASP-2, but only a minor fraction of MAp19, was associated with PRMs. In contrast to previous reports we found that MAp19 could not compete with MASP-2 for binding to MBL, nor could it inhibit MASP-2-mediated complement activation. Immunohistochemical analyses combined with qRT-PCR revealed that both MAp19 and MASP-2 were mainly expressed in hepatocytes. High levels of MAp19 were found in urine, where MASP-2 was absent.
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