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Human CD59 Protein expressed in Human Cells - ABIN2005233
Fletcher, Harrison, Lachmann, Neuhaus: Structure of a soluble, glycosylated form of the human complement regulatory protein CD59. in Structure (London, England : 1993) 1994
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Nonfunctioning CD59 is a major risk factor for stroke and hypercoagulability.
Therapeutic strategies that seek to modulate the functions of CD59 in the tumor microenvironment could be a promising direction for tumor immunotherapy.
Movement of Domain 2 with respect to Domain 3 of ILY is essential for forming a late prepore intermediate that releases CD59, while the role of cholesterol may be limited to insertion of the transmembrane segments. Together these data define a structural timeline for ILY pore formation and suggest a mechanism that is relevant to understanding other pore-forming toxins that also require CD59.
CD59 polymorphisms are associated with gene expression and different sexual susceptibility to pemphigus foliaceus (show DSG1 Proteins) in the Brazilian patients.
we demonstrated that CD59 regulation by SOX2 (show SOX2 Proteins) is required for stem cell evasion of complement surveillance. This finding highlights the importance of complement surveillance in eliminating CSCs and may suggest CD59 as a potential target for cancer therapy.
The results indicate that shear stress is an important mediator in endothelial progenitor cells expression of CD59 regulated by the extacellular matrix-integrin alphaVbeta3-F-actin pathway, which is a key factor in preventing membrane attack complex-mediated cell autolysis.
Data show that following 4 patients with CD59 Cys89Tyr mutations who are treated with eculizumab, no strokes occurred and non-permanent neurological insults underwent resolution without any new neurological exacerbations.
our results indicate that the Lys (show LYZ Proteins)(41) /His(44) glycation motif in human CD59 may confer humans a higher risk of developing vascular disease in response to hyperglycemia.
Structural basis for receptor recognition by the human CD59-responsive cholesterol-dependent cytolysins has been presented.
developed a model of conditional and targeted cell ablation by generating floxed STOP-CD59 knockin mice (ihCD59), in which expression of human CD59 only occurs after Cre-mediated recombination
Data demonstrate that the resistance of neonatal porcine Sertoli cells to human xenoantibody and complement-mediated lysis is associated with low expression of xenoantigen alpha-Gal and high production of the complement inhibitors clusterin (show CLU Proteins) and CD59.
This gene encodes a cell surface glycoprotein that regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. This protein also plays a role in signal transduction pathways in the activation of T cells. Mutations in this gene cause CD59 deficiency, a disease resulting in hemolytic anemia and thrombosis, and which causes cerebral infarction. Multiple alternatively spliced transcript variants, which encode the same protein, have been identified for this gene.
, 20 kDa homologous restriction factor
, CD59 antigen p18-20 (antigen identified by monoclonal antibodies 16.3A5, EJ16, EJ30, EL32 and G344)
, CD59 glycoprotein
, Ly-6-like protein
, MEM43 antigen
, T cell-activating protein
, human leukocyte antigen MIC11
, lymphocytic antigen CD59/MEM43
, membrane attack complex (MAC) inhibition factor
, membrane attack complex inhibition factor
, membrane inhibitor of reactive lysis
, surface anitgen recognized by monoclonal antibody 16.3A5
, CD59 antigen
, CD59b moleucle, complement regulatory protein
, Cb59b molecule
, MAC-inhibitory protein
, CD59 homolog
, CD59 molecule, complement regulatory protein