MYH13 Double Nickase Plasmid (h): sc-400602-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MYH13 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
- MYH13 Double Nickase Plasmid (h) and MYH13 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MYH13. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYH13 Double Nickase Plasmid (h) | sc-400602-NIC | 20 µg | $410.00 | |||
MYH13 Double Nickase Plasmid (h2) | sc-400602-NIC-2 | 20 µg | $410.00 |
MYH13 encodes myosin heavy chain 13, a fast skeletal muscle–specific motor protein that functions as the ATP-dependent force generator within the actin–myosin sarcomere. As a core component of thick filaments, MYH13 contributes to muscle contraction kinetics, myofibril organization, and regulation of contractile fiber properties through actomyosin cross-bridge cycling. Its expression pattern links it to pathways governing skeletal muscle differentiation, sarcomere assembly, and excitation–contraction coupling. Altered myosin heavy chain composition and sarcomeric dysfunction are implicated in neuromuscular and myopathic phenotypes, making MYH13 a relevant target for studying mechanisms of muscle function and disease-associated contractile defects.
MYH13 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MYH13 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MYH13. 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 MYH13 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 MYH13-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.