Product Description
Natural human C5ais prepared from human C5 protein cleaved into C5a and C5b by human C5 convertase.The C5a is converted to C5a desArg by proteolytic removal of the C-terminal arginine.The primary carboxypeptidase responsible for Arg removal is serum carboxypeptidase N, but there are several different carboxypepticases in serum.C5a desArg is a naturally glycosylated polypeptide containing 73 amino acids with a molecular weight of approx. 10,250 daltons.It contains 25% carbohydrate attached to a single Asn residue at position 64. This carbohydrate is of variable structure leading to a broad distribution of MW upon analysis by mass spectroscopy.C5a is the most potent anaplylatoxin (compared to C3a and C4a).C5a desArg is produced when C5a is “inactivated” by removal of its C-terminal arginine amino acid.This cleavage occurs by the action of the plasma enzyme carboxypeptidase N.This inactivation is rapid and most C5a is converted to C5a desArg within minutes of its formation.“Inactivated” C5a still possesses approx. 1% of its anaphylatoxic and chemotatic activities, but its stimulatory activity is only reduced 10-fold.Thus, C5a desArg retains considerable biological activity even though it is frequently called inactivated C5a.Its biological properties include being weakly chemotactic for neutrophils (PMN), causing smooth muscle contraction, increasing vascular permeability, causing histamine and TNF-alpharelease, and causing lysosomal degranulation of immune cells.C5a and C5a desArg act through the C5a Receptor (C5aR, CD88, a G-protein coupled receptor) on PMN, monocytes, alveolar macrophages, and mast cells.A second receptor of unknown function (C5L2, gpr77) has been identified.Due to the widespread expression of C5a receptors and the results from C5aR KO mice it is believed that C5a and its receptors have many non-immunolgical functions in organ development, CNS development, neurodegeneration, tissue regeneration and hematopoiesis (Monk, P.N. et al. (2007)).
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Complement Technology的C1是级联反应中的第一个补体成分,称为补体经典途径。C1与抗原结合的抗体(免疫复合物)结合并被其激活,从而产生引发级联反应的蛋白酶。C1实际上是钙依赖性复合物中结合在一起的三种不同蛋白质(C1q,C1r和C1s)的非共价复合物。C1q通过其六个臂中的两个或多个与IgG或IgM的Fc结构域结合。多臂与免疫复合物的结合被认为会引入压力,从而导致复合物中的两个C1r蛋白(蛋白酶酶原)自身激活,从而产生两种活性的C1r丝氨酸蛋白酶(Morikis,D.和Lambris,JD(2005))。 。这些激活的C1r亚基裂解并激活复合物中的两个C1s蛋白酶酶原。活化的C1裂解补体成分C4,释放出C4a,并启动C4b与活化表面的共价连接。活化的C1也切割C2,并且C2的较大片段结合至表面附着的C4b,形成C4b,C2a,其为经典途径的C3 / C5转化酶。

