MTAP Double Nickase Plasmid (h): sc-406223-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MTAP 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
- MTAP Double Nickase Plasmid (h) and MTAP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MTAP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MTAP Antibody (42-T): sc-100782
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MTAP Double Nickase Plasmid (h) | sc-406223-NIC | 20 µg | $410.00 | |||
MTAP Double Nickase Plasmid (h2) | sc-406223-NIC-2 | 20 µg | $410.00 |
MTAP (methylthioadenosine phosphorylase) is a key enzyme in the methionine salvage pathway that catalyzes phosphorolysis of 5′-methylthioadenosine generated during polyamine biosynthesis. By recycling methionine and adenine, MTAP contributes to nucleotide homeostasis, methylation potential, and cellular metabolic balance, linking purine metabolism with one-carbon and polyamine-related processes. Loss or reduced expression of MTAP is frequently observed in genomic regions adjacent to CDKN2A/B and is widely studied for its impact on tumor-associated metabolic dependencies and altered methylation networks. MTAP perturbation is therefore relevant to investigations of metabolic reprogramming, epigenetic regulation, and stress-adaptive signaling in human cells.
MTAP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MTAP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MTAP. 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 MTAP 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 MTAP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.