Human Insulin ELISA Kit, fluorescent (ab278125)
Key features and details
- One-wash 90 minute protocol
- Sensitivity: 8.04 pmol/L
- Range: 13.28 pmol/L - 425 pmol/L
- Sample type: EDTA Plasma, Hep Plasma, Serum
- Detection method: Fluorescent
- Assay type: Sandwich (quantitative)
- Reacts with: Human
Overview
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Product name
Human Insulin ELISA Kit, fluorescent
See all Insulin kits -
Detection method
Fluorescent -
Precision
Intra-assay Sample n Mean SD CV% Serum 8 9.4% Inter-assay Sample n Mean SD CV% Serum 3 11.8% -
Sample type
Serum, Hep Plasma, EDTA Plasma -
Assay type
Sandwich (quantitative) -
Sensitivity
8.04 pmol/L -
Range
13.28 pmol/L - 425 pmol/L -
Recovery
Sample specific recovery Sample type Average % Range Serum 96 94% - 98% Hep Plasma 89 80% - 97% EDTA Plasma 99 95% - 103% -
Assay time
1h 30m -
Assay duration
One step assay -
Species reactivity
Reacts with: Human -
Product overview
Human Insulin in vitro CatchPoint® SimpleStep ELISA® (Enzyme-Linked Immunosorbent Assay) kit is designed for the quantitative measurement of Insulin protein in human serum, plasma heparin, and plasma EDTA samples.
This CatchPoint SimpleStep ELISA kit has been optimized for Molecular Devices Microplate Readers. Click here for a list of recommended Microplate Readers.
If using a Molecular Devices’ plate reader supported by SoftMax® Pro software, a preconfigured protocol for these CatchPoint SimpleStep ELISA Kits is available with all the protocol and analysis settings at www.softmaxpro.org
The CatchPoint SimpleStep ELISA employs an affinity tag labeled capture antibody and a reporter conjugated detector antibody which immunocapture the sample analyte in solution. This entire complex (capture antibody/analyte/detector antibody) is in turn immobilized via immunoaffinity of an anti-tag antibody coating the well. To perform the assay, samples or standards are added to the wells, followed by the antibody mix. After incubation, the wells are washed to remove unbound material. CatchPoint HRP Development Solution containing the Stoplight Red Substrate is added. During incubation, the substrate is catalyzed by HRP generating a fluorescent product. Signal is generated proportionally to the amount of bound analyte and the intensity is measured in a fluorescence plater reader at 530/570/590 nm Excitation/Cutoff/Emission.
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Notes
Insulin is a highly conserved, secreted hormone essential for glucose metabolism. Produced by pancreatic beta cells, proinsulin is proteolyzed into an A and a B chain, which form a 6 kDa mature protein. Basal levels of insulin are continuously delivered into the bloodstream, and additional levels are secreted proportional to food ingestion. Insulin secretion is highly regulated, and dysregulation of insulin production or sensitivity results in Type 1 diabetes mellitus or Type 2 diabetes mellitus, respectively.
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Platform
Microplate (12 x 8 well strips)
Properties
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Storage instructions
Store at +4°C. Please refer to protocols. -
Components 1 x 96 tests 100X Stoplight Red Substrate 1 x 120µl 10X Human Insulin Capture Antibody 1 x 600µl 10X Human Insulin Detector Antibody 1 x 600µl 10X Wash Buffer PT (ab206977) 1 x 20ml 500X Hydrogen Peroxide (H2O2, 3%) 1 x 50µl Antibody Diluent CPI - HAMA Blocker (ab193969) 1 x 6ml Human Insulin Lyophilized Recombinant Protein 2 vials Plate Seals 1 unit Sample Diluent NS (ab193972) 1 x 12ml SimpleStep Pre-Coated Black 96-Well Microplate 1 unit Stoplight Red Substrate Buffer 1 x 12ml -
Research areas
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Function
Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver. -
Involvement in disease
Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:176730].
Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:125852]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:606176]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.
Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:613370]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease. -
Sequence similarities
Belongs to the insulin family. -
Cellular localization
Secreted. - Information by UniProt
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Alternative names
- IDDM
- IDDM1
- IDDM2
see all -
Database links
- Entrez Gene: 3630 Human
- Omim: 176730 Human
- SwissProt: P01308 Human
- Unigene: 272259 Human
Images
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Catchpoint ELISA Protocol Diagram
SimpleStep ELISA technology allows the formation of the antibody-antigen complex in one single step, reducing assay time to 90 minutes. Add samples or standards and antibody mix to wells all at once, incubate, wash, and add your final substrate. See protocol for a detailed step-by-step guide.
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Example of human Insulin standard curve in Sample Diluent NS.The Insulin standard curve was prepared as described in Section 10. Raw data generated on SpectraMax M4 Multi-Mode Microplate Reader is shown in the table. Background-subtracted data values (mean +/- SD) are graphed.
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Recombinant Antibody BenefitsTo learn more about the advantages of recombinant antibodies see here.
Datasheets and documents
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SDS download
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Datasheet download
References (0)
ab278125 has not yet been referenced specifically in any publications.