Aprataxin Double Nickase Plasmid (h): sc-417083-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Aprataxin 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
- Aprataxin Double Nickase Plasmid (h) and Aprataxin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting APTX. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Aprataxin Antibody (B-12): sc-374108
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Aprataxin Double Nickase Plasmid (h) | sc-417083-NIC | 20 µg | $410.00 | |||
Aprataxin Double Nickase Plasmid (h2) | sc-417083-NIC-2 | 20 µg | $410.00 |
Human APTX encodes aprataxin, a DNA repair factor that resolves abortive DNA ligation intermediates by removing adenylate groups from 5′ DNA termini, thereby restoring ligatable ends during single-strand break repair. Aprataxin functions in genome maintenance pathways linked to PARP-dependent repair signaling, coordination with XRCC1–DNA ligase III complexes, and protection against replication-associated damage. Loss of APTX activity compromises repair of oxidative and topoisomerase-induced lesions, promoting accumulation of strand breaks and elevated genomic instability. APTX dysfunction is associated with neurodegenerative phenotypes, making it a relevant target for studying DNA damage responses in neuronal and dividing cell contexts.
Aprataxin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the APTX locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within APTX. 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 APTX 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 APTX-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.