Human DMD Knockout Cell Line-HeLa
Cat.No. : CSC-RT0606
Host Cell: HeLa Target Gene: DMD
Size: 1x10^6 cells/vial, 1mL Validation: Sequencing
Inquire for Price
Cell Line Information
Cell Culture Information
Safety and Packaging
| Cat. No. | CSC-RT0606 |
| Cell Line Information | A stable cell line with a homozygous knockout of human DMD using CRISPR/Cas9. |
| Target Gene | DMD |
| Host Cell | HeLa |
| Shipping | 10^6 cells/tube |
| Storage | Liquid nitrogen |
| Species | Human |
| Gene ID | 1756 |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Media Type | Cells were cultured in DMEM supplemented with 10% fetal bovine serum. |
| Growth Properties | Cells are cultured as a monolayer at 37°C in a humidified atmosphere with 5% CO2. Split at 80-90% confluence, approximately 1:4-1:6. |
| Freeze Medium | Complete medium supplemented with 10% (v/v) DMSO |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
Inquiry
Background
Applications
The dystrophin gene (DMD) is one of the longest known human genes, spanning approximately 2.4 megabases of DNA sequence. The DMD gene is located on the X chromosome at the Xp21.2 locus and is responsible for encoding dystrophin, a key protein involved in the structural integrity of muscle cells. Dystrophin is a key component of a protein complex that connects the internal cytoskeleton of the muscle fiber to the surrounding extracellular matrix through the cell membrane. This connection is essential for maintaining muscle cell stability during cycles of contraction and relaxation.
Mutations in the DMD gene can cause muscular dystrophies, a group of muscle wasting disorders, the most severe of which is Duchenne muscular dystrophy (DMD). Duchenne muscular dystrophy affects approximately 1 in 3,500 to 5,000 live male births worldwide as it primarily affects males due to its X-linked recessive inheritance pattern. Females can be carriers of the mutation and may display milder symptoms. Loss or dysfunction of dystrophin due to the mutation leads to progressive muscle degeneration, resulting in symptoms such as muscle weakness, walking impairment, and severe cardiopulmonary complications. Early diagnosis is often facilitated by symptoms observed in early childhood, elevated serum creatine kinase levels, and genetic testing.
Human Duchenne Muscular Dystrophy Knockout Cell Line - HeLa refers to HeLa cells in which the dystrophin gene (DMD) has been knocked out. Here are some of the key applications:
Duchenne Muscular Dystrophy Research: DMD Knockout HeLa cells help study Duchenne Muscular Dystrophy (DMD) to better understand the molecular mechanisms and pathways involved in the disease. This helps identify potential targets for therapeutic intervention.
Drug Screening and Development: DMD Knockout HeLa cells can be used to screen for new drugs that can improve or treat symptoms associated with DMD. The lack of dystrophin in these cells allows for the evaluation of compounds for efficacy and toxicity.
Protein Interaction Studies: Researchers can study how the lack of dystrophin affects other protein interactions within the cell. This can reveal new insights into cellular processes disrupted by the mutation and identify secondary targets for treatment.
Pathway Analysis: Using these knockout cells, scientists can analyze changes in signaling pathways and cellular responses due to the loss of dystrophin.
For research use only. Not intended for any clinical use.
