C5788
Complement C5a 人
recombinant, expressed in E. coli, ~95% (SDS-PAGE), lyophilized powder
别名:
C5a Anaphylatoxin, rC5a
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关于此项目
Form:
lyophilized powder
Assay:
~95% (SDS-PAGE)
Biological source:
human
Recombinant:
expressed in E. coli
Application
Complement C5a human is an important terminal component of the complement cascade. It is a direct mediator of inflammation, and has been identified as a novel biomarker for pain and inflammation following surgery
Biochem/physiol Actions
A mixture of C5a (~35%) and C5a having an added methionyl residue at the amino terminus (~65%); exhibits biological activities similar to serum-derived C5a. C5a is a (11.2kDa) proteolytic fragment of the C5 α-chain through the action of C5 convertases in the classical and alternative complement pathway (C4b2a4b, C3bBb3b). C5a is an anaphylatoxin. It acts as an inflammatory chemoattractant. C5a stimulation of human neutrophils leads to STAT3 phosphorylation on Ser727. It mediates IL-8 release from bronchial epithelial cells. C5a anaphylatoxin activity on hepatocytes results indirectly from interaction with nonparenchymal cell via prostanoid secretion.
C5a, in addition to being a direct mediator of inflammation, can induce both IL-8 (interleukin-8) synthesis and high levels of IL-8 release from monocytes. This secondary effect serves as an amplification mechanism for inflammation at sites of infection or trauma. C5a exerts its effect through a G-protein coupled receptor, CD88.
Analysis Note
Mol. Wt.: ~8.6 kDa (non-glycosylated, with glutathione attached to cysteine 27).
Other Notes
View more information on the complement pathway at www.sigma-aldrich.com/enzymeexplorer
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
法规信息
新产品
此项目有
Markus Bosmann et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 27(12), 5010-5021 (2013-08-29)
We investigated how complement activation promotes tissue injury and organ dysfunction during acute inflammation. Three models of acute lung injury (ALI) induced by LPS, IgG immune complexes, or C5a were used in C57BL/6 mice, all models requiring availability of both
Andrea L Conroy et al.
Cell host & microbe, 13(2), 215-226 (2013-02-19)
Placental malaria (PM) is a major cause of fetal growth restriction, yet the underlying mechanism is unclear. Complement C5a and C5a receptor levels are increased with PM. C5a is implicated in fetal growth restriction in non-infection-based animal models. In a
Julia Phieler et al.
Journal of immunology (Baltimore, Md. : 1950), 191(8), 4367-4374 (2013-09-18)
Obese adipose tissue (AT) inflammation contributes critically to development of insulin resistance. The complement anaphylatoxin C5a receptor (C5aR) has been implicated in inflammatory processes and as regulator of macrophage activation and polarization. However, the role of C5aR in obesity and
J David Clark et al.
Anesthesiology, 104(6), 1274-1282 (2006-05-30)
Activation of the complement system is one component of the inflammatory response. Various components of the complement system participate in killing foreign organisms, recruiting immune cells, enhancing edema, and stimulating cytokine formation. Complement-mediated enhancement of the inflammation surrounding surgical incisions
A Conway Morris et al.
British journal of anaesthesia, 111(5), 778-787 (2013-06-13)
Nosocomial infection occurs commonly in intensive care units (ICUs). Although critical illness is associated with immune activation, the prevalence of nosocomial infections suggests concomitant immune suppression. This study examined the temporal occurrence of immune dysfunction across three immune cell types
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