SMC2 Double Nickase Plasmid (h): sc-411488-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SMC2 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
- SMC2 Double Nickase Plasmid (h) and SMC2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SMC2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SMC2 Double Nickase Plasmid (h) | sc-411488-NIC | 20 µg | $410.00 |
SMC2 encodes a core structural maintenance of chromosomes protein that forms the ATPase scaffold of the condensin complexes, which drive chromosome condensation and organization during mitosis and meiosis. By regulating higher-order chromatin architecture, SMC2 supports faithful sister chromatid resolution, segregation, and genome stability, linking its activity to cell-cycle progression and DNA damage responses. Condensin-dependent chromatin compaction intersects with replication stress and repair pathways, where altered condensin function can promote chromosomal instability and aneuploidy. Dysregulation of SMC2 expression or function has been observed in proliferative disease contexts, making it a useful node for studying mitotic fidelity and genome maintenance mechanisms in human cells.
SMC2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SMC2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SMC2. 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 SMC2 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 SMC2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.