Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
dystrophin Double Nickase Plasmid (h): sc-400657-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- dystrophin Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- dystrophin Double Nickase Plasmid (h) and dystrophin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DMD. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: dystrophin Antibody (7A10): sc-47760
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
dystrophin Double Nickase Plasmid (h) | sc-400657-NIC | 20 µg | $410.00 | |||
dystrophin Double Nickase Plasmid (h2) | sc-400657-NIC-2 | 20 µg | $410.00 |
DMD encodes dystrophin, a large cytoskeletal protein that anchors the actin network to the dystrophin–glycoprotein complex at the sarcolemma, stabilizing muscle fibers during contraction. Through its role in linking intracellular cytoskeleton to extracellular matrix, dystrophin contributes to membrane integrity, mechanotransduction, and organization of costameres in skeletal and cardiac muscle. Loss or reduction of dystrophin disrupts these structural and signaling interactions, altering calcium handling, inflammatory signaling, and muscle regeneration programs. DMD dysfunction is strongly associated with X-linked muscular dystrophies, making dystrophin a central node for studying muscle degeneration mechanisms and genotype–phenotype relationships in human models.
dystrophin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DMD locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DMD. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt DMD function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of DMD-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.