MicroVue™ Ba EIA
The MicroVue Ba Enzyme Immunoassay Kit measures the amount of the complement fragment Ba in human urine, plasma or serum.
Product Specifications
Citations | 31 |
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Specimen |
Serum 10 μL, EDTA Plasma 25 μL, Urine 10 μL |
LLOQ | 0.033 ng/mL |
ULOQ | 3.239 ng/mL |
Assay Time | 2.5 hours |
Cross Reactivity |
African Green Monkey, Cynomolgous monkey, Dog, Rhesus monkey |
Ordering Information
Catalog Number | A033 |
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Catalog Number (CE) | A034 |
Size | 96 wells/test |
Price (USD) | $725.00 |
Price (EURO) | 640,00 € |
Contact us
US Phone | +1 (858) 552 1100 |
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EU Phone | +353 (91) 412 474 |
US Email | contact-us@quidelortho.com |
EU Email | contact-emea@quidelortho.com |
- Specifications
- Citations
- Certificate of Analysis
Specifications
Description |
The MicroVue Ba Enzyme Immunoassay Kit measures the amount of the complement fragment Ba in human urine, plasma or serum. |
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Size | 96 wells/test |
Form |
96 well plate with 12 eight-well strips in a resealable foil pouch |
Specimen | Serum 10 μL, EDTA Plasma 25 μL, Urine 10 μL |
Limit of Detection (LOD) | 0.011 ng/mL |
Lower Limit of Quantitation (LLOQ) | 0.033 ng/mL |
Upper Limit of Quantitation (ULOQ) | 3.239 ng/mL |
Intra Assay | 2.2–3.3% |
Inter Assay | 2.4–8.1% |
Standards | 5 |
Controls | 2 |
Sample Values |
Serum 436–3362 ng/mL, EDTA Plasma 226–2153 ng/mL, Urine 0.6–27.0 ng/mL |
Assay Time | 2.5 hours |
Cross Reactivity |
African Green Monkey, Cynomolgous monkey, Dog, Rhesus monkey |
Storage |
Store the unopened kit at 2°C to 8°C. Refer to Product Insert for additional storage details. |
Background |
Measurement of Ba in human urine, plasma or serum provides evidence of the involvement of the alternative pathway of complement. The alternative complement pathway provides innate protection against microbial agents in the absence of specific antibody. The activation of this complement pathway can be triggered by a variety of substances including microbial polysaccharides or lipids, gram-negative bacterial lipopolysaccharides, and surface determinants present on some viruses, parasites, virally infected mammalian cells, and cancer cells. In autoimmune diseases, the alternative complement pathway may contribute directly to tissue damage. A centrally important reaction that occurs during alternative pathway activation is the conversion of the 93 Kd molecular weight Factor B zymogen to an active proteolytic enzyme. This is accomplished in a two-step reaction. During the first reaction step the Factor B forms a magnesium-dependent complex with C3(H20) or C3b. The C3(H20),B complex is formed only in fluid-phase while the C3b,B complex can be formed either in fluid-phase or on a target surface. Factor B, which is present in the C3(H20),B or the C3b,B complex, is cleaved into the Ba (33 Kd) and Bb (60 Kd) fragments in the second reaction step by the alternative pathway enzyme, Factor D. Although alternative pathway activation is thought to occur primarily in the absence of specific antibody, many situations arise in which alternative pathway activation can occur as the result of classical pathway activation. For example, immune complexes that are present in autoimmune disease patients can trigger classical complement pathway activation with resultant production of C3b fragments. As described above, these C3b molecules are capable of binding Factor B and initiating its cleavage into the Ba and Bb fragments. Thus, alternative pathway activation can occur in antibody-mediated autoimmune disease states and may contribute significantly to enhanced complement activation and concomitant tissue destruction. By assessing Factor B cleavage products in test specimens, one can estimate the extent of alternative pathway utilization occurring at the time of sample collection in the disease state under investigation. The MicroVue Ba EIA provides a simple, rapid, non-radioactive, highly specific, and quantitative procedure for measuring Factor B activation. It is ideal for investigations involving the role or status of the alternative complement pathway in numerous research and clinical settings and for monitoring the generation of Ba in vitro. |
Citations
Title | Year | Applications | Sample Species | Sample | Sample Details |
---|---|---|---|---|---|
2015 | ELISA |
Human |
GMVEC cells, HUVEC cells |
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2018 | ELISA |
Human |
GMVEC cells, BMVEC cells |
||
Intravascular hemolysis activates complement via cell-free heme and heme-loaded microvesicles. |
2018 | ELISA |
Human |
Serum |
Microvesicles with heme |
2019 | ELISA |
Human |
Aqueous humour |
Age-Related Macular Degeneration |
|
Complement fragments are biomarkers of antibody-mediated endothelial injury. |
2019 | ELISA |
Human |
Plasma |
Antibody-mediated endothelial injury |
Local complement activation is associated with primary graft dysfunction after lung transplantation. |
2020 | ELISA |
Human |
Bronchoalveolar lavage |
Lung transplant |
Complement Activation in the Vitreous of Patients With Proliferative Diabetic Retinopathy. |
2020 | ELISA |
Human |
Plasma, Vitreous Humor |
Proliferative Diabetic Retinopathy |
2020 | ELISA |
Human |
Serum |
Lupus Nephritis, Thrombotic Microangiopathy |
|
2020 | ELISA |
Human |
Urine |
Lupus Nephritis, Thrombotic Microangiopathy |
|
Complement Expression and Activation in Osteoarthritis Joint Compartments. |
2020 | ELISA |
Human |
Chondrocytes |
Supernatent |
Complement Expression and Activation in Osteoarthritis Joint Compartments. |
2020 | ELISA |
Human |
Synoviocytes |
Supernatent |
Establishing a Case for Anti-complement Therapy in Membranous Nephropathy. |
2020 | ELISA |
Human |
Urine |
Membranous Nephropathy |
Increased complement activation is a distinctive feature of severe SARS-CoV-2 infection |
2021 | ELISA |
Human |
Plasma |
COVID-19 |
2021 | ELISA |
Human |
Plasma |
IgA Nephropathy |
|
2021 | ELISA |
Human |
Plasma |
Thrombotic Microangiopathy - TA |
|
Increased complement activation is a distinctive feature of severe SARS-CoV-2 infection. |
2021 | ELISA |
Human |
Plasma |
COVID-19 |
2022 | ELISA |
Human |
Plasma |
COVID-19 |
|
2022 | ELISA |
Human |
Serum |
COVID-19 |
|
2022 | ELISA |
Human |
Plasma |
Heat-related illnesses |
|
2022 | ELISA |
Human |
Complement Proteins |
||
Comparison of Complement Pathway Activation in Autoimmune Glomerulonephritis. |
2022 | ELISA |
Human |
Urine |
AAV, FSGS, IgAN, MN, and LN |
2022 | ELISA |
Human |
Plasma |
Age-Related Macular Degeneration |
|
2022 | ELISA |
Human |
Plasma |
IgA Nephropathy |
|
2023 | ELISA |
Human |
Plasma, Serum |
Glomerulonephritis |
|
Human factor H-related protein 2 (CFHR2) regulates complement activation |
2013 | ELISA |
Human |
Serum |
|
Defining the complement biomarker profile of C3 glomerulopathy |
2014 | ELISA |
Human |
Plasma |
C3G |
2015 | ELISA |
Human |
ARPE-19 Cells |
||
2015 | ELISA |
Human |
Serum |
||
2017 | ELISA |
Human |
Serum |
ARMS2 protein |
|
Persistent complement dysregulation with signs of thromboinflammation in active Long Covid. |
2023 | ELISA |
Human |
Serum |
COVID-19 |
Persistent complement dysregulation with signs of thromboinflammation in active Long Covid |
2024 | ELISA |
Human |
Serum |
COVID-19 |