SNM1A Double Nickase Plasmid (h): sc-411393-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SNM1A 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
- SNM1A Double Nickase Plasmid (h) and SNM1A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting DCLRE1A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SNM1A Double Nickase Plasmid (h) | sc-411393-NIC | 20 µg | $410.00 | |||
SNM1A Double Nickase Plasmid (h2) | sc-411393-NIC-2 | 20 µg | $410.00 |
DCLRE1A encodes SNM1A, a 5′–3′ exonuclease of the metallo-β-lactamase family that promotes repair of DNA interstrand crosslinks and other lesions that stall replication forks. SNM1A functions downstream of the Fanconi anemia pathway and cooperates with structure-specific endonucleases to process crosslink-derived DNA intermediates, supporting replication-coupled repair and genome stability. By limiting replication stress and chromosomal aberrations, SNM1A contributes to cellular responses to genotoxic damage and maintenance of proliferative capacity. Altered DCLRE1A/SNM1A activity has been linked to impaired DNA damage tolerance and susceptibility to genome instability phenotypes relevant to cancer biology and inherited DNA repair disorders.
SNM1A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the DCLRE1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within DCLRE1A. 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 DCLRE1A 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 DCLRE1A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.