APNG Double Nickase Plasmid (h): sc-404850-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- APNG 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
- APNG Double Nickase Plasmid (h) and APNG Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MPG. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: APNG Antibody (D-2): sc-390684
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APNG Double Nickase Plasmid (h) | sc-404850-NIC | 20 µg | $410.00 |
Human MPG encodes N-methylpurine DNA glycosylase (APNG/AAG), a key initiating enzyme in the base excision repair (BER) pathway that recognizes and excises alkylated and deaminated purine lesions such as 3-methyladenine and hypoxanthine. By generating abasic sites that are further processed by AP endonucleases, polymerases, and ligases, APNG helps maintain genome stability during replication and in response to endogenous and environmental DNA damage. MPG activity intersects with cellular responses to oxidative stress and replication stress, influencing mutation accumulation and chromosomal integrity. Dysregulated BER capacity, including altered APNG function or expression, has been linked to genomic instability phenotypes observed across multiple disease-associated contexts, making MPG a useful target for mechanistic DNA repair studies.
APNG Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MPG locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MPG. 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 MPG 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 MPG-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.