CD59


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CD59

a glycosylphosphatidylinositol-anchored membrane protein present on many hemopoietic cells, vascular endothelium, epithelial cells, and placenta that inhibits membrane complement attack and may be involved in T-cell signal transduction; absent or defective in paroxysmal nocturnal hemoglobinuria.

CD59

A 65-kD membrane, glycosyl-phosphatidylinositol-anchored complement-neutralising protein encoded by CD59 on chromosome 11p13, which inhibits the complement membrane attack complex, binding to C8 and C9 during assembly of the complex.

Normal expression
Most leukocytes and red cells.

Abnormal expression
May be absent in some forms of paroxysmal nocturnal haemoglobinuria.
References in periodicals archive ?
reported in a ROC curve analysis that a panel consisting of 5 proteins (M2BP, MRP14, CD59, catalase, and profilin) had a sensitivity of 90% and a specificity of 83% in the diagnosis of the OSCC via LC-MS/MS [155].
No modifications of the membrane regulators, DAF, CR1, and CD59, were observed in case of Bothrops venoms exposure [28, 30-32].
This expression period allowed the cells to recover from the temporary growth lag after ZnO NP treatment and to multiply such that the progeny of the mutated cells no longer expressed lethal amounts of CD59 surface antigen.
Handa, "Oxidized low-density-lipoprotein-induced injury in retinal pigment epithelium alters expression of the membrane complement regulatory factors CD46 and CD59 through exosomal and apoptotic bleb release," Advances in Experimental Medicine and Biology, vol.
In our study we found new protease inhibitors including inter-alpha-trypsin inhibitor (AMBP-Human), inhibitor of the complement membrane attack complex (CD59) and proteases including mannan-binding lectin serine protease 2 (MASP2_Human).
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).
LU domain-containing proteins have evolved to serve multiple diverse physiologic functions, for example, inhibition of autologous complement activation, CD59 [3]; driving cell surface-associated plasminogen activation, uPAR [4]; localizing intravascular triglyceride hydrolysis on capillaries, GPIHBP1 [5, 6]; regulating fertility, TEX101 [7]; and neutrophil function, CD177 [8].
Erythrocyte autoantibodies and expression of CD59 on the surface of red blood cells of polytransfused patients with betathalassemia major.
"And the second arm (CD59) inhibits a specific part of the complement system which would drive further damage if left unchecked.
The absence of CD59 from platelets leads to thrombin generation, an increased sensitivity to aggregation by thrombin and increased risk of thrombosis.
Transcription analysis of 44 CD genes was also carried out, indicating 24 CD genes (CD3E, CD244, CD69, CD247, CD40L, CD38, CD5L, CD44, CD5, CD83, CD163L1, CD36, CD14, CD28, CD200R1A, CD40, CD59, CD200, CD4, CD2, CD72, CD180, CD79B, and CD93) to be markedly increased by 2.1- to 8.4-fold, and 4 CD genes (CD163, CD8A, CD34, and CD7) to be significantly decreased by 2.1- to 8.2-fold in chicken line 6.3 with p < 0.01 and fold [greater than or equal to] 2.