INT45109
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
C5A is capable of causing granulocyte/granulocyte interactions that lead to clumping, vasoocclusion, and the extension of infarctive damage in patients with coronary artery disease. | |||||||||||||||
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The mechanism of action seems to be associated with the inhibition of local anaphylatoxin release (C3a and C5a) which are responsible for the acute evolution of the lesions produced by viruses of the Zoster-Varicella group and with a quick lethal effect on the parasitized cells which are selectively eliminated without affecting the adjoining normal cells of the host. | |||||||||||||||
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Neutrophil influx and phagocytosis are inhibited by CHIPS, which binds the C5aR, and ScpA that cleaves C5a. | |||||||||||||||
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C5a binds to its G protein-coupled receptor (C5aR) on polymorphonuclear leukocytes (PMNLs) through a high-affinity helical bundle and a low-affinity C terminus, the latter being solely responsible for receptor activation. | |||||||||||||||
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C5a binds to its G protein-coupled receptor (C5aR) on polymorphonuclear leukocytes (PMNLs) through a high-affinity helical bundle and a low-affinity C terminus, the latter being solely responsible for receptor activation. | |||||||||||||||
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Structure-activity relationships for 60 cyclic analogs were evaluated by competitive radioligand binding with C5a (affinity) and myeloperoxidase release (antagonist potency) from human PMNLs, with 20 compounds having high antagonist potencies (IC(50), 20 nM-1 microM). | |||||||||||||||
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C5a binds to its G protein-coupled receptor (C5aR) on polymorphonuclear leukocytes (PMNLs) through a high-affinity helical bundle and a low-affinity C terminus, the latter being solely responsible for receptor activation. | |||||||||||||||
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C5a exerts its activities by binding to the G-protein-coupled C5a receptor on the plasma membrane of target cells. | |||||||||||||||
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C5a exerts its activities by binding to the G-protein-coupled C5a receptor on the plasma membrane of target cells. | |||||||||||||||
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To confirm the in vitro results in an in vivo model, Matrigel plugs supplemented with PBS (controls), FGF-2, C5a, or C3a were implanted subcutaneously into mice. | |||||||||||||||
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These results suggested that C5a could participate in the vascularization and accumulation of adipocytes around inflamed vessels. | |||||||||||||||
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C5a is associated with various diseases [38], but efforts to develop antagonists have not yet been successful. | |||||||||||||||
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C5 convertases cleave C5 into the anaphylatoxin C5a, which attracts neutrophils to the site of infection, and C5b, which forms a complex with complement proteins C6C9 to generate the membrane attack complex | |||||||||||||||
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C5 convertases cleave C5 into the anaphylatoxin C5a, which attracts neutrophils to the site of infection, and C5b, which forms a complex with complement proteins C6C9 to generate the membrane attack complex | |||||||||||||||
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General Comments
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