Dystrophin ELISA Kit (RMEK-0151388)
Cat. No.: RMEK-0151388
Category: ELISA Kits
INQUIRY
1 x 96 tests
Human Dystrophin ELISA kit is a single-wash 90 min sandwich ELISA designed for the quantitative measurement of Human Dystrophin protein in human and mouse cell and tissue extract samples. The technology employs capture antibodies conjugated to an affinity tag that is recognized by the monoclonal antibody used to coat our plates. This approach to sandwich ELISA allows the formation of the antibody-analyte sandwich complex in a single step, significantly reducing assay time.
Product Features
| Species Reactivity | Mouse, Human |
|---|---|
| Detection Method | Colorimetric |
| Assay Duration | One step assay |
| Assay Time | 1.5 h |
| Assay Type | Sandwich (quantitative) |
| Precision | Intra-Assay-Extract-8-3.4%; Inter-Assay-Extract-0-0% |
| Sensitivity | 15.12 pg/mL |
| Range | 117.188 pg/mL - 7500 pg/mL |
| Sample Type | Cell Lysate, Tissue |
| Recovery | Tissue Extracts-112%; Cell Lysate-118% |
| Key Features | One-wash 90 minute protocol; Sensitivity: 15.12 pg/mL; Range: 117.188 pg/mL - 7500 pg/mL; Sample type: Cell Lysate, Tissue; Detection method: Colorimetric; Assay type: Sandwich (quantitative); Reacts with: Mouse, Human |
Target Information
| Target Symbol | DMD |
|---|---|
| UniProt ID | P11532 |
| Biomarker of SCs/CSCs | Luminal A Breast Cancer |
| Function | Anchors the extracellular matrix to the cytoskeleton via F-actin. Ligand for dystroglycan. Component of the dystrophin-associated glycoprotein complex which accumulates at the neuromuscular junction (NMJ) and at a variety of synapses in the peripheral and central nervous systems and has a structural function in stabilizing the sarcolemma. Also implicated in signaling events and synaptic transmission. |
| Cellular Localization | Cell membrane > sarcolemma. Cytoplasm > cytoskeleton. |
| Involvement in Disease | Defects in DMD are the cause of Duchenne muscular dystrophy (DMD). DMD is the most common form of muscular dystrophy; a sex-linked recessive disorder. It typically presents in boys aged 3 to 7 year as proximal muscle weakness causing waddling gait, toe-walking, lordosis, frequent falls, and difficulty in standing up and climbing up stairs. The pelvic girdle is affected first, then the shoulder girdle. Progression is steady and most patients are confined to a wheelchair by age of 10 or 12. Flexion contractures and scoliosis ultimately occur. About 50% of patients have a lower IQ than their genetic expectations would suggest. There is no treatment. Defects in DMD are the cause of Becker muscular dystrophy (BMD). BMD resembles DMD in hereditary and clinical features but is later in onset and more benign. Defects in DMD are a cause of cardiomyopathy dilated X-linked type 3B (CMD3B); also known as X-linked dilated cardiomyopathy (XLCM). Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death. |
Storage & Shipping
| Storage | Store at 2-8°C |
|---|---|
| Shipping | Gel Packs |
| Stability | The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. |
For research use only. Not for clinical use.
