C3BCPEDB Configuration Control Board
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In addition, activated microglia secretes the proinflammatory cytokines IL-1[beta] and IL-18.Astrocytes stimulated by inflammatory signals secrete C3 that is cleaved into C3b and C3a.
As indicated before, C3 cleaves into different products including C3a and C3b. C3b cleavage product iC3b binds to CR3 [24, 25], whereas C3a binds to C3aR [14].
The following are primary antibodies: antigranulocye colonystimulating factor (G-CSF), anti-Von Willebrand factor (vWF), and leukocyte common antigen, CD45 (Clone I3/ 2.3), came from Abcam (Cambridge, MA); anti-neutrophil (NIMP14) antibody came from Novus Biologicals (Littleton, CO); C3b/iC3b/C3c (C3b) came from Hycult Biotechnology (Uden, Netherlands); anticluster of differentiation, CD68, was from AbD Serotec (Raleigh, NC); and antiplatelet endothelial cell adhesion molecule (PECA1)/CD31 was from Genetex (Irvine, CA).
Since C3 is cleaved to C3a and C3b by the contact of the surface with blood, irrespective of whether the activation occurs via classical or alternative pathways, and also C3a could be adsorbed on to the material surface just like any other proteins, C3 depletion in the medium can be taken as an indirect measure of complement activation.
APL-2 is a synthetic cyclic peptide conjugated to a polyethylene glycol polymer that binds specifically to C3 and C3b, effectively blocking all three pathways of complement activation (classical, lectin, and alternative).
Low CR1 (C3b receptor) level on erythrocytes is associated with poor prognosis in hemodialysis patients.
In the alternative complement pathway, C3b reacts with the proteins factor B, adipsin, and properdin to compose C3 convertase.
Rodriguez et al., "Zinc-induced self-association of complement C3b and factor H: implications for inflammation and age-related macular degeneration," The Journal of Biological Chemistry, vol.
Rudolph et al., "Combined C3b and factor B autoantibodies and MPGN type II," New England Journal of Medicine, vol.
The replacement of nickel for magnesium leads to a 40-fold increase in the formation of C3b, Bb enzyme, which amplifies activation of the complement pathway.
Acute and prolonged activation of complement proteins (C3a, C3b, C5, and C5a) is seen in CSF of patients with HSE but not healthy controls [40].