E01M0350 Human Mucin 5 subtype AC ELISA kit
The Human Mucin 5 subtype AC ELISA kit can be used to identify samples from the human species. Mucin 5 subtype AC can also be called MUC5AC, TBM, MUC5, LeB, Oligomeric Mucus/Gel-Forming, Mucin 5, Subtypes A and C, Tracheobronchial/Gastric, Gastric mucin, Lewis B blood group antigen, Major airway glycoprotein, Mucin-5 subtype AC, tracheobronchial, Tracheobronchial mucin, TBM.
Product Information | |
Cat. No. | E01M0350 |
Product Name | Human Mucin 5 subtype AC ELISA kit |
Species | Human |
Product Size | 48 Tests / 96 Tests |
Concentration | 1.0-25 ng/ml |
Sensitivity | 0.1 ng/ml |
Principal | Competitive ELISA |
Sample Volume | 100 ul |
Sample Type | Serum, plasma, cell culture supernatants, body fluid and tissue homogenate |
Assay Time | 90 minutes |
Platform | Microplate Reader |
Conjugate | HRP |
Detection Method | Colorimetric |
Storage | 2-8°C |
Kit Components | ||
MATERIALS | SPECIFICATION | QUANTITY |
MICROTITER PLATE | 96 wells | stripwell |
ENZYME CONJUGATE | 6.0 mL | 1 vial |
STANDARD A (0.5mL) | 0 ng/mL | 1 vial |
STANDARD B (0.5mL) | 1.0 ng/mL | 1 vial |
STANDARD C (0.5mL) | 2.5 ng/mL | 1 vial |
STANDARD D (0.5mL) | 5.0 ng/mL | 1 vial |
STANDARD E (0.5mL) | 10 ng/mL | 1 vial |
STANDARD F (0.5mL) | 25 ng/mL | 1 vial |
SUBSTRATE A | 6 mL | 1 vial |
SUBSTRATE B | 6 mL | 1 vial |
STOP SOLUTION | 6 mL | 1 vial |
WASH SOLUTION (100 x) | 10 mL | 1 vial |
BALANCE SOLUTION | 3 mL | 1 vial |
Principle of the Assay |
MUC5AC ELISA kit uses an anti-MUC5AC antibody and an MUC5AC-HRP conjugate in a competitive enzyme immunoassay method. MUC5AC-HRP conjugate is incubated with the assay sample and buffer in a pre-coated plate for one hour. The wells are decanted and washed five times when the incubation period is over. The HRP enzyme substrate is then incubated in the wells. The result of the enzyme-substrate reaction is a complex that is blue in hue. The process is finally stopped by adding a stop solution, causing the solution to turn yellow. In a microplate reader, the color intensity is measured spectrophotometrically at 450 nm. Due to competition for the anti-MUC5AC antibody binding site between MUC5AC from samples and MUC5AC-HRP conjugate, the intensity of the color is inversely proportional to the concentration of MUC5AC. Since the number of sites is limited, as more sites are occupied by MUC5AC from the sample, fewer sites are left to bind MUC5AC-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The MUC5AC concentration in each sample is interpolated from this standard curve. |
Coefficient of Variance | Intra Variation% ＜10% | |
Inter Variation% ＜12% | ||
Recovery | 95-102% | |
Linearity | Diluent Ratio | Range % |
1:2 | 93-105 | |
1:4 | 88-106 | |
1:8 | 86-108 | |
Specificity/Cross-reactivity | No significant cross-reactivity or interference between MUC5AC and analogues was observed. | |
E01M0350 has been referenced in the below publications：
TMEM16A-Mediated Mucin Secretion in IL-13-Induced Nasal Epithelial Cells From Chronic Rhinosinusitis Patients.
Proteomic Profiles in Acute Respiratory Distress Syndrome Differentiates Survivors from Non-Survivors.
IL-13 inhibits differentiation of human nasal ciliated epithelial cells.
Long Noncoding RNA Linc00632 Inhibits Interleukin-13-Induced Inflammatory Cytokine and Mucus Production in Nasal Epithelial Cells.
IL-19 Up-Regulates Mucin 5AC Production in Patients With Chronic Rhinosinusitis via STAT3 Pathway.
Epidermal growth factor upregulates expression of MUC5AC via TMEM16A, in chronic rhinosinusitis with nasal polyps.
ATF4-mediated GDF15 suppresses LPS-induced inflammation and MUC5AC in human nasal epithelial cells through the PI3K/Akt pathway.
miR-143 inhibits interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from allergic rhinitis patients by targeting IL13Rα1.
Prunetin inhibits lipopolysaccharide-induced inflammatory cytokine production and MUC5AC expression by inactivating the TLR4/MyD88 pathway in human nasal epithelial cells.
Tripterine alleviates lipopolysaccharide-induced airway epithelial barrier dysfunction through suppressing the Hippo pathway.
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