Myosin Ia Double Nickase Plasmid (h): sc-404995-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Myosin Ia 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
- Myosin Ia Double Nickase Plasmid (h) and Myosin Ia Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MYO1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Myosin Ia Double Nickase Plasmid (h) | sc-404995-NIC | 20 µg | $410.00 | |||
Myosin Ia Double Nickase Plasmid (h2) | sc-404995-NIC-2 | 20 µg | $410.00 |
Human MYO1A encodes myosin Ia, an actin-dependent motor protein enriched at the apical surface of epithelial cells where it supports brush border architecture and membrane–cytoskeleton coupling. Myosin Ia contributes to cortical actin dynamics, vesicle trafficking, and polarized transport processes that help maintain microvillar organization and epithelial barrier function. Through its roles in cytoskeletal remodeling and membrane tension regulation, MYO1A is relevant to pathways governing cell polarity, adhesion, and epithelial homeostasis. Altered MYO1A expression or function has been associated with epithelial dysfunction and has been studied in the context of gastrointestinal biology and disease-associated changes in epithelial differentiation.
Myosin Ia Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MYO1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MYO1A. 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 MYO1A 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 MYO1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.