MIRL

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MIRL

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It was suggested that chronic arterial thrombosis secondary to autoimmunity may be the main cause of MMS formation.[2],[3] In PNH patient, deficiency of two important complement regulatory proteins on cell surfaces, CD55 and CD59, makes blood cells more sensitive and vulnerable to the action of complement response.
These include antigens from the Cartwright, Dombrock, Cromer, JMH, and CD59 blood group systems.
Other glycated proteins such as glycated fibronectin and glycated pregnancy-specific glycoprotein (PSG), glycated complement regulatory protein CD59, plasma fatty acid binding protein 4 (FABP4), plasma retinol binding protein 4 (RBP4), and plasma adipocytokine are being investigated for their potential to diagnose GDM without the need for fasting and oral glucose administration.
The characterization of IFP-MSCs is based on the presence of cell markers such as CD9, CD10, CD13, CD29, CD44, CD49e, CD59, CD105, CD106, and CD166 [104].
On the other hand, different investigations mainly based on Western blot, or MRS-based targeted proteomics techniques have found cell-surface glycoproteins overexpressed in patients with OSCC such as CD44, CD59, or CEA.
Finally, neuroglia express inhibitory protective molecules to prevent uncontrolled complement-mediated damage, such as CD59, complement factor H (CFH), and complement receptor-related protein-y (Crry), which mainly interfere with C3 [19, 117].
The activation of the Complement cascade is regulated by membrane proteins including Complement-receptor 1 (CR1), membrane cofactor protein (MCP/CD46), decay-accelerating factor (DAF/CD55), and CD59. Factor I, Factor H, Factor-H related proteins, C4-binding protein (C4BP), and C1inhibitor (C1-INH) are important soluble regulators of Complement [23-26].
Thrombophilia screen included protein S, protein C, antithrombin, paroxysmal nocturnal hemoglobinuria (flow cytometry with CD55, CD59, and fluoresce-in-labeled proaerolysin (FLAER) expression), and JAK2 mutation.
Age-Related Macular Degeneration (AMD): The complement regulatory protein CD59 reduces membrane attack complex formation, considered one of the causes of AMD, by 62%.
Tenders are invited for Supply of Diagnostic Kits and making a Rate Contract for 2 years: Alpha Naphthylamine Solution,Moeller Arginine decarboxylase broth,Ceruloplasmin Control,Hha1 (Enzyme),Anti CD59 Antibody (Rabbit Polyclonal) conc.
AL cells are sensitive to the cytotoxic effects of monoclonal E7.1 antibodies, which are specific to the CD59 antigen located on human chromosome 11 [38].
Exosomes remain relatively stable in the blood as they avoid coagulation factors and complement which are most likely due to their surface expression of CD46 and CD59 [84], as well as antibody responses, due to their self-derived nature.