MicroVue™ iC3b EIA

The MicroVue iC3b Assay is enzyme immunoassay for the quantitation of iC3b fragment of C3 protein.


Product Specifications

Citations12
Specimen

Serum/EDTA or Heparin Plasma 100 μL

LLOQN/A
ULOQN/A
Assay Time1.5 hours
Cross Reactivity

None

Ordering Information

For Research Use Only in the United States. Not for use in diagnostic procedures.
Catalog NumberA006
Catalog Number (CE) 
Size96 wells/test
Price (USD)$725.00
Price (EURO)640,00 €

Contact us

US Phone+1 (858) 552 1100
EU Phone+353 (91) 412 474
US Emailcontact-us@quidelortho.com
EU Emailcontact-emea@quidelortho.com

Specifications

Description

The MicroVue iC3b Assay is enzyme immunoassay for the quantitation of iC3b fragment of C3 protein.

Size96 wells/test
Form

96 well plate with 12 eight-well strips in a resealable foil pouch

SpecimenSerum/EDTA or Heparin Plasma 100 μL
Limit of Detection (LOD)N/A
Lower Limit of Quantitation (LLOQ)N/A
Upper Limit of Quantitation (ULOQ)N/A
Intra AssayN/A
Inter AssayN/A
Standards3
Controls2
Sample Values

None

Assay Time1.5 hours
Cross Reactivity

None

Storage

Store the unopened kit at 2°C to 8°C. Refer to Product Insert for additional storage details.

Background

The Quidel iC3b Enzyme Immunoassay measures the amount of the iC3b present in samples. Activation of either complement pathway results in the assembly of C3 convertases that cleave C3 into two fragments – C3a and C3b. The C3a fragment is one of the complement anaphylatoxins. The C3b fragment has many important biological activities, including the promotion of phagocytosis by opsonization and participation as a structural component in C3 and C5 convertases. These biological activities of C3b are under stringent control in vivo. One mechanism limiting the in vivo lifetime of C3b involves the two-site cleavage of C3b by Factor I5 with the cooperation of Factor H6 or CR17 as cofactors. Factor H is a complement control protein. CR1 is the C3b/C4b receptor found on many cell types, including red blood cells, granulocytes, monocytes, and macrophages. Factor I two-site cleavage of C3b yields inactivated C3b, called iC3b. The biological activities of C3b are lost when it is cleaved by Factor I. iC3b fragments, either in fluid phase or bound to biological surfaces, express new biological activities due to their ability to interact with CR2 and CR3 receptors on a variety of cell types. The levels of iC3b can be significantly elevated in the serum and plasma of some patients with immune complex-associated diseases such as rheumatoid arthritis and systemic lupus erythematosus. iC3b levels may also be elevated in body fluids from other patients in which complement activation is known to occur, e.g., from patients with infections, burns, myocardial infarctions, glomerulonephritis, and acute respiratory distress syndrome. The correlation between iC3b levels and the clinical status or prognosis for patients with these and other diseases remains to be determined and is a question of potential significance to the biomedical community. The Quidel iC3b Enzyme Immunoassay provides a rapid, non-radioactive, highly specific and quantitative procedure for measuring this product of C3 activation. It may also be used as a research tool to monitor the generation of iC3b in vitro.

Citations

TitleYearApplicationsSample SpeciesSampleSample Details

Complement receptor 3 mediates Aspergillus fumigatus internalization into alveolar epithelial cells with the increase of intracellular phosphatidic acid by activating FAK.

2021ELISAHuman

Serum

Aspergillus incubated

Effect of Aerobic and Anaerobic Exercise on the Complement System of Proteins in Healthy Young Males.

2020ELISAHuman

Plasma

N/A

A monoclonal antibody targeting amyloid β (Aβ) restores complement factor I bioactivity: Potential implications in age-related macular degeneration and Alzheimer's disease

2018ELISAHuman

Plasma

Age-Related Macular Degeneration

A monoclonal antibody targeting amyloid β (Aβ) restores complement factor I bioactivity: Potential implications in age-related macular degeneration and Alzheimer's disease

2018ELISAHuman

Plasma

Alzheimer's Disease

Complement Receptor 3 Has Negative Impact on Tumor Surveillance through Suppression of Natural Killer Cell Function

2017ELISAHuman

Serum

N/A

quantitative lateral flow assay to detect complement activation in blood.

2015ELISAHuman

Plasma

N/A

Cerebrospinal fluid inflammatory markers in patients with Listeria monocytogenes meningitis

2014ELISAHuman

CSF

Listeria meningitis

C4d deposits on the surface of RBCs in trauma patients and interferes with their function

2014ELISAHuman

Serum

Trauma

Inhibition of C3 Convertase Activity by Hepatitis C Virus as an Additional Lesion in the Regulation of Complement Components

2014ELISAHuman

Serum

HCV

Genetic variation and cerebrospinal fluid levels of mannose binding lectin in pneumococcal meningitis patients

2013ELISAHuman

CSF

N/A

Macrophage scavenger receptor A mediates the uptake of gold colloids by macrophages in vitro

2011ELISAHuman

Plasma

N/A

Complement activation by bisretinoid constituents of RPE lipofuscin.

2009ELISAHuman

Serum

N/A