MYL3 Double Nickase Plasmid (m): sc-421787-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MYL3 Double Nickase Plasmid (m) 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
- MYL3 Double Nickase Plasmid (m) and MYL3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Myl3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MYL3 Antibody (MLM527): sc-58804
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYL3 Double Nickase Plasmid (m) | sc-421787-NIC | 20 µg | $410.00 | |||
MYL3 Double Nickase Plasmid (m2) | sc-421787-NIC-2 | 20 µg | $410.00 |
Myl3 encodes myosin light chain 3 (MYL3), an essential regulatory component of striated muscle myosin that stabilizes the lever arm and tunes actin–myosin cross-bridge cycling during contraction. In mouse cardiac and slow-twitch skeletal muscle, MYL3 contributes to sarcomere assembly, contractile kinetics, and mechanotransduction in pathways linking calcium handling, myofibrillar organization, and energy demand. Perturbation of MYL3 levels or sequence alters sarcomeric performance and has been associated with cardiomyopathy-related phenotypes and broader myofibrillar dysfunction. As a result, Myl3 is widely used in studies of muscle development, contractility, and genotype-to-phenotype relationships in striated muscle disease models.
MYL3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Myl3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Myl3. 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 Myl3 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 Myl3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.