Human G-CSF enzyme-linked immunoassay kit
| Specification | 96 Test |
|---|---|
| Sensitivity | 0.61 pg/ml (50 μl)；10.62 pg/ml (10 μl) |
| Standard Curve Range | 8.19~2000 pg/ml |
| Standard Curve Gradient | 7 Points |
| Number of Incubations | 2 |
| Sample Volume | 50 μl/10 μl |
| Type | Fully Ready-to-Use |
| Operation Duration | 120min |
| pg/ml | O.D. | Average | Corrected | |
|---|---|---|---|---|
| 0.00 | 0.0148 | 0.0144 | 0.0146 | |
| 8.19 | 0.0336 | 0.0353 | 0.0345 | 0.0199 |
| 20.48 | 0.0645 | 0.0670 | 0.0658 | 0.0512 |
| 51.20 | 0.1376 | 0.1524 | 0.1450 | 0.1304 |
| 128.00 | 0.3456 | 0.3250 | 0.3353 | 0.3207 |
| 320.00 | 0.8238 | 0.8329 | 0.8284 | 0.8138 |
| 800.00 | 1.7270 | 1.9720 | 1.8495 | 1.8349 |
| 2000.00 | 3.5990 | 3.7930 | 3.6960 | 3.6814 |
Precision
| Intra-assay Precision | Inter-assay Precision | |||||
| Sample Number | S1 | S2 | S3 | S1 | S2 | S3 |
| 22 | 22 | 22 | 6 | 6 | 6 | |
| Average(pg/ml) | 49.6 | 227.9 | 737.9 | 43.6 | 210.6 | 661.4 |
| Standard Deviation | 2.9 | 6.7 | 49.3 | 1.2 | 9.5 | 18.9 |
| Coefficient of Variation(%) | 5.9 | 2.9 | 6.7 | 2.6 | 4.5 | 2.9 |
Intra-assay Precision (Precision within an assay) Three samples of known concentration were tested twenty times on one plate to assess intra-assay precision.
Inter-assay Precision (Precision between assays) Three samples of known concentration were tested six times on one plate to assess intra-assay precision.
Spike Recovery
The spike recovery was evaluated by spiking 3 levels of human G-CSF into health human serum sample. The un-spiked serum was used as blank in this experiment.
The recovery ranged from 80% to 119% with an overall mean recovery of 101%.
Sample Values
| Sample Matrix | Sample Evaluated | Range (pg/ml) | Detectable (%) | Mean of Detectable (pg/ml) |
|---|---|---|---|---|
| Serum | 30 | 0.72-42.44 | 100 | 6.93 |
Serum/Plasma – Thirty samples from apparently healthy volunteers were evaluated for the presence of G-CSF in this assay. No medical histories were available for the donors.
Product Data Sheet
Background: G-CSF
Granulocyte-colony stimulating factor (G-CSF) is a 24-25 kDa monomeric glycoprotein that regulates the proliferation, differentiation, and activation of hematopoietic cells in the neutrophilic granulocyte lineage. Mature human G-CSF is a 178 amino acid (aa) O-glycosylated protein that contains two intrachain disulfide bridges. In humans, alternate splicing generates a second minor isoform with a 3 aa deletion. Mouse and human G-CSF share 76% aa sequence identity, and the two proteins show species cross-reactivity. G-CSF is produced by activated monocytes and macrophages, fibroblasts, endothelial cells, astrocytes, neurons, and bone marrow stroma cells. In addition, various tumor cells express G-CSF constitutively. Human G-CSF receptor (G-CSF R) is a 120 kDa type I transmembrane glycoprotein that belongs to the hematopoietin receptor superfamily. The mature protein consists of a 603 aa extracellular domain (ECD), a 23 aa transmembrane segment, and a 186 aa cytoplasmic domain. The ECD contains an N-terminal Ig-like domain, a cytokine receptor homology domain, and three fibronectin type III domains. Alternate splicing of human G-CSF R generates additional isoforms including a potentially soluble form of the receptor. The ECDs of mouse and human G-CSF R share 63% aa sequence identity. G-CSF R forms a complex with the ligand in a 2:2 ratio. It is expressed on monocytes, neutrophils, megakaryocytes, platelets, myeloid progenitors, trophoblasts and placenta, endothelial cells, and various tumor cell types. G-CSF is an important regulator for granulopoiesis in vivo, and mutations in G-CSF R are associated with congenital neutropenia. G-CSF can support the growth of multilineage hematopoietic progenitor cells and mobilize them from the bone marrow into the bloodstream. G-CSF enhances the functional capacity of mature neutrophils and supports their survival by limiting the rate of apoptosis. G-CSF also enhances M-CSF induced monocytopoiesis from hematopoietic progenitor cells and stimulates the proliferation of peripheral Th2-inducing dendritic cells. It promotes the development of T cell immune tolerance as well as tissue recovery following myocardial infarction and cerebral ischemia.
