CD55

CD55

a glycosylphosphatidylinositol-anchored membrane protein present on all hemopoietic cells and spermatozoa that neutralizes complement activation; absent or defective in paroxysmal nocturnal hemoglobinuria.
References in periodicals archive ?
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.
Cromer is located on decay accelerating factor (DAF, CD55) which inhibits assemblage of C3 and C5 converting enzymes of the classical and alternative pathways.
Clusters 1 and 2 are characterized by significant overexpression of genes responsible for extracellular matrix remodeling and cell recruitment (for example, matrix metalloproteinase 3 (Mmp3; p < [10.sup.-7]), collagen 1a2 (Col1a2; p < [10.sup.-4]), and stromal cell factor 1 (Cxcl12/Sdf1; p < [10.sup.-3]) (Figure 2(a)) as well T cell and complement activation (dipeptyl-peptide4 (Dpp4/Cd26; p < [10.sup.-7]) and Cd55; p < [10.sup.-6]) (Figure 2(b)).
Kirschfink, "Lipoplex mediated silencing of membrane regulators (CD46, CD55 and CD59) enhances complement-dependent anti-tumor activity of trastuzumab and pertuzumab," Molecular Oncology, vol.
The following murine antibodies against human CD46 (clone E4.3), CD55 (clone IA10), and CD59 (clone p282-H19) were purchased from BD Pharmingen (San Diego, CA, USA).
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.
Paroxysmal nocturnal hemoglobinuria (PNH) is a complex hematologic disorder characterized by an acquired somatic mutation in the phosphatidylinositol glycan (PIG-A) gene resulting in a deficiency of the glycosyl phosphatidylinositol (GPI) anchored proteins, particularly CD55 and CD59 on the cell membrane [1].
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, X-linked blood disorder in which red blood cells lack the GPI-APs CD55 and CD59 due to somatic mutations in a gene (phosphatidylinositol glycan class A, PIGA).
Of the PLC samples, we found that the transcriptional expressions of MLH3, ACSL6, CD55, CR1, PDE3B, CCNB1, PAICS, SEC62, BIRC3, TCF7, NT5E, and PSPH in the PBMCs of gan-shen Yin deficiency group were significantly lower than those in non-gan-shen Yin deficiency group (Figure 1(a), p < 0.05).
Since the first report for Gal deficiency pig production using SCNT [3], various transgenic pigs with multiple genes modifications including CD39, CD55, CD59, endothelial protein C receptor, and thrombomodulin were generated for xenotransplantation [4].
ID MARKET $/GAL ID A CONTRACTOR 15.0 Ac15 A CONTRACTOR 17.5 Ac17 A DIY 25.0 Ad25 A DIY 42.0 Ad42 B CONTRACTOR 22.5 Bc22 B CONTRACTOR 42.0 Bc42 B DIY 42.1 Bd42 B DIY 44.8 Bd44 C CONTRACTOR 12.6 Cc12 C CONTRACTOR 20.6 Cc20 C DIY 21.6 Cd21 C DIY 55.4 Cd55 D CONTRACTOR 40.4 Dc40 D CONTRACTOR 41.6 Dc41 D DIY 40.6 Dd40 D DIY 69.8 Dd69 TABLE 2--Painting Experience Evaluation STRONGLY DISAGREE DISAGREE STEADY 1.
In view of initial reports showing hemolysis and presence of cerebral sinus thrombus, a rare differential diagnosis of PNH was kept and flow cytometry was performed on granulocytes and RBCs, revealing that 95.6% granulocytes and 94% of RBCs were negative for CD55.