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C1163

Sigma-Aldrich

Complement C5 deficient serum human

for complement assays

NACRES:
NA.61

biological source

human

Quality Level

form

solution

technique(s)

activity assay: suitable

UniProt accession no.

storage temp.

−70°C

Gene Information

human ... C5(727)

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This Item
C1288C1413C2910
form

solution

form

liquid

form

solution

form

solution

technique(s)

activity assay: suitable

technique(s)

activity assay: suitable

technique(s)

activity assay: suitable

technique(s)

activity assay: suitable

UniProt accession no.

P01031

UniProt accession no.

P13671

UniProt accession no.

P10643

UniProt accession no.

P01024

storage temp.

−70°C

storage temp.

−70°C

storage temp.

−70°C

storage temp.

−70°C

Quality Level

200

Quality Level

200

Quality Level

200

Quality Level

200

Application

Complement C5 deficiencies in humans are rare, but often associated with recurrent infections by Neisseria spp. (such as meningitis). Deficiency in C5 results in an impairment of hemolytic activity from both the classical and alternative pathway of the complement system. Recently, genetic research has revealed that a 153 bp deletion in exon 30 results in complete C5 deficiency. Research has also implicated C5 deficiency in a predisposition to cardiac dysfunction when cardiac injury occurs.

Biochem/physiol Actions

Complement C5 deficiency can, paradoxically, protect against certain effects of infection. Patients deficient in C5 are unusually susceptible to meningococcal infection, but have a milder course of infection. Reduced expression of tumor necrosis factor (TNF) may account for this effect.

Physical form

Supplied as a solution in PBS, pH 7.4

Analysis Note

C5 is depleted by immunoadsorption as determined by hemolytic assay.

Storage Class Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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A novel role for the fifth component of complement (C5) in cardiac physiology.
Mullick A., et al.
PLoS ONE, 6 (2011)
Magda R Hamczyk et al.
Methods in molecular biology (Clifton, N.J.), 1339, 235-246 (2015-10-09)
The key roles of macrophages in atherosclerosis include the phagocytosis of apoptotic and necrotic cells and cell debris, whose accumulation in atherosclerotic lesions exacerbates inflammation and promotes plaque vulnerability. Evidence is accumulating that macrophage phagocytic functions peak at the early
Taku Fukuzawa et al.
Scientific reports, 7(1), 1080-1080 (2017-04-26)
Dysregulation of the complement system is linked to the pathogenesis of a variety of hematological disorders. Eculizumab, an anti-complement C5 monoclonal antibody, is the current standard of care for paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS). However
Robert Lodge et al.
PloS one, 7(3), e32761-e32761 (2012-03-14)
Over the past decade, the number of reported human immunodeficiency virus type-1 (HIV-1)/Leishmania co-infections has risen dramatically, particularly in regions where both diseases are endemic. Although it is known that HIV-1 infection leads to an increase in susceptibility to Leishmania
Kelly Mulfaul et al.
The Journal of pathology, 257(1), 29-38 (2022-01-18)
Activation of the alternative complement pathway is an initiating event in the pathology of age-related macular degeneration (AMD). Unchecked complement activation leads to the formation of a pro-lytic pore, the membrane attack complex (MAC). MAC deposition is observed on the

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