Smarcad1 Double Nickase Plasmid (m): sc-420234-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Smarcad1 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
- Smarcad1 Double Nickase Plasmid (m) and Smarcad1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Smarcad1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Smarcad1 Double Nickase Plasmid (m) | sc-420234-NIC | 20 µg | $410.00 | |||
Smarcad1 Double Nickase Plasmid (m2) | sc-420234-NIC-2 | 20 µg | $410.00 |
Mouse Smarcad1 encodes an ATP-dependent chromatin remodeling factor of the SNF2 family that helps regulate nucleosome dynamics during DNA replication and repair. SMARCAD1 participates in chromatin reassembly at replication forks, promotes end resection at double-strand breaks, and supports homologous recombination while limiting aberrant recombination events. Through interactions with replication- and repair-associated complexes, it influences transcriptional regulation, heterochromatin maintenance, and genome stability. Altered SMARCAD1 function has been linked to defects in DNA damage responses and epigenetic regulation, making it relevant for studies of genomic instability, developmental phenotypes, and cancer-associated chromatin dysregulation.
Smarcad1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Smarcad1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Smarcad1. 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 Smarcad1 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 Smarcad1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.