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C3b helps bring about the elimination of the microbial invader in two ways: Bound C3b activates the formation of membrane attack complexes, structures composed of other complement proteins that poke holes into the membrane of the invading microorganism and allow the contents of the cell to leak out and the cell to die.
The complement system is activated by both antibodies (classical pathway) and microorganisms (lectin and alternative pathways) leading to the formation of membrane attack complexes (C5b-9), which lyse and destroy target cells.
Human leukemic cells remove membrane attack complexes from their surfaces by phosphorylating C9 [ 92].
Complement C3 is activated in urine via pH and urea, resulting in formation of membrane attack complexes on the epithelial side of tubular cells [ 28].
Also, flow cytometry experiments with antibodies recognizing neo-epitope within C5b-9 reveal strong augmentation in incorporated membrane attack complexes (MAC) in Raji cells preincubated with sorafenib.
In addition, C3b binds to other proteins on the surface of pathogens, forming membrane attack complexes which clear foreign pathogens [ 13].
Similar(52)
Membrane attack complex is required for accelerated rejection induced by previous preganancy.
Anaphylatoxins and assembly of the membrane attack complex contribute directly and indirectly to further tissue damage.
(v) CD59: CD59 is a complement regulatory protein that acts by inhibiting formation of the membrane attack complex.
Upregulation of the majority of the complement cascade was observed including the membrane attack complex components and complement inhibitors.
A recent study suggested a role for the complement membrane attack complex in experimental models of osteoarthritis.
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