Nori Human COL3A1 ELISA Kit
$508.00 – $916.00
This ELISA kit is for quantification of COL3A1 in human. This is a quick ELISA assay that reduces time to 50% compared to the conventional method, and the entire assay only takes 3 hours. This assay employs the quantitative sandwich enzyme immunoassay technique and uses biotin-streptavidin chemistry to improve the performance of the assays. An antibody specific for COL3A1 has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any COL3A1 present is bound by the immobilized antibody. After washing away any unbound substances, a detection antibody specific for COL3A1 is added to the wells. Following wash to remove any unbound antibody reagent, a detection reagent is added. After intensive wash a substrate solution is added to the wells and color develops in proportion to the amount of COL3A1 bound in the initial step. The color development is stopped, and the intensity of the color is measured.
Alternative names for COL3A1: Collagen type III alpha 1, alpha-1 type III collagen, Collagen III alpha 1,
This product is for laboratory research use only not for diagnostic and therapeutic purposes or any other purposes.
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Description
Nori Human COL3A1 ELISA Kit Summary
Alternative names for COL3A1: Collagen type III alpha 1, alpha-1 type III collagen, Collagen III alpha 1,
| Assay Type | Solid Phase Sandwich ELISA |
| Format | 96-well Microplate or 96-Well Strip Microplate |
| Method of Detection | Colorimetric |
| Number of Targets Detected | 1 |
| Target Antigen Accession Number | P02461 |
| Assay Length | 3 hours |
| Quantitative/Semiquantitative | Quantitative |
| Sample Type | Plasma, Serum, Cell Culture, Urine, Cell/Tissue Lysates, Synovial Fluid, BAL, |
| Recommended Sample Dilution (Plasma/Serum) | No dilution for sample <ULOQ; sufficient dilution for samples >ULOQ |
| Sensitivity | 120 pg/mL |
| Detection Range | 625-40000 pg/mL |
| Specificity | Human COL3A1 |
| Cross-Reactivity | < 0.5% cross-reactivity observed with available related molecules, < 50% cross-species reactivity observed with species tested. |
| Interference | No significant interference observed with available related molecules |
| Storage/Stability | 4 ºC for up to 6 months |
| Usage | For Laboratory Research Use Only. Not for diagnostic or therapeutic use. |
| Additional Notes | The kit allows for use in multiple experiments. |
Standard Curve
Kit Components
1. Pre-coated 96-well Microplate
2. Biotinylated Detection Antibody
3. Streptavidin-HRP Conjugate
4. Lyophilized Standards
5. TMB One-Step Substrate
6. Stop Solution
7. 20 x PBS
8. Assay Buffer
Other Materials Required but not Provided:
1. Microplate Reader capable of measuring absorption at 450 nm
2. Log-log graph paper or computer and software for ELISA data analysis
3. Precision pipettes (1-1000 µl)
4. Multi-channel pipettes (300 µl)
5. Distilled or deionized water
Protocol Outline
1. Prepare all reagents, samples and standards as instructed in the datasheet.
2. Add 100 µl of Standard or samples to each well and incubate 1 h at RT.
3. Add 100 µl of Working Detection Antibody to each well and incubate 1 h at RT.
4. Add 100 µl of Working Streptavidin-HRP to each well and incubate 20 min at RT.
5. Add 100 µl of Substrate to each well and incubate 5-30 min at RT.
6. Add 50 µl of Stop Solution to each well and read at 450 nm immediately.
Background:
Type III Collagen is a homotrimer, or a protein composed of three identical peptide chains (monomers), each called an alpha 1 chain of type III collagen (COL3A1) that is encoded by the COL3A1 gene. [1] Type III collagen is one of the fibrillar collagens whose proteins have a long, inflexible, triple-helical domain.[1] Type III collagen is found as a major structural component in hollow organs such as large blood vessels, uterus and bowel. It is also found in many other tissues together with type I collagen. Mutations in the COL3A1 gene cause Ehlers-Danlos syndrome, vascular type (vEDS or the EDS type IV). It is the most severe form of EDS, since patients often die suddenly due to rupture of large arteries or other hollow organs.[2] A few patients with arterial aneurysms without clear signs of EDS have also been found to have COL3A1 mutations.[3] More recently, mutations in COL3A1 have also been identified in patients with severe brain anomalies suggesting that type III collagen is important for the normal development of the brain during embryogenesis.[4] Type III collagen could also be important in several other human diseases. Increased amounts of type III collagen are found in many fibrotic conditions such as liver and kidney fibrosis, and systemic sclerosis.[5][6] This has led to a search for serum biomarkers that could be used for diagnosing these conditions without having to obtain a tissue biopsy. The most widely used biomarker is the N-terminal propeptide of type III procollagen, which is cleaved off during the biosynthesis of type III collagen.[7]
References
- Kuivaniemi H, Tromp G (2019). Gene. 707: 151–171.
- Jørgensen A, et al. (2015). European Journal of Human Genetics. 23 (6): 796–802.
- Kontusaari S, et al. (1990). The Journal of Clinical Investigation. 86 (5): 1465–73.
- Horn D, et al. (2017). American Journal of Medical Genetics. Part A. 173 (9): 2534–2538.
- Krieg T, et al. (1986). The Journal of Investigative Dermatology. 87 (6): 788–91.
- Jimenez SA, et al. (1986). The Biochemical Journal. 237 (3): 837–43.
- Risteli J, et al. (1988). Clinical Chemistry. 34 (4): 715–8.
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