MSH2 Double Nickase Plasmid (h): sc-400966-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MSH2 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
- MSH2 Double Nickase Plasmid (h) and MSH2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MSH2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MSH2 Antibody (D-6): sc-376384
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MSH2 Double Nickase Plasmid (h) | sc-400966-NIC | 20 µg | $410.00 | |||
MSH2 Double Nickase Plasmid (h2) | sc-400966-NIC-2 | 20 µg | $410.00 |
MSH2 encodes a core component of the DNA mismatch repair (MMR) machinery that recognizes base–base mismatches and insertion/deletion loops arising during DNA replication and recombination. As part of the MutSα (MSH2–MSH6) and MutSβ (MSH2–MSH3) complexes, MSH2 initiates lesion processing that couples mismatch recognition to excision and resynthesis, thereby preserving genome stability. MSH2 function intersects with DNA damage response signaling and influences replication stress outcomes and mutation rates. Altered MSH2 activity is strongly associated with microsatellite instability and hypermutator phenotypes that are widely studied in hereditary and sporadic tumor biology.
MSH2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MSH2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MSH2. 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 MSH2 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 MSH2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.