APOBEC3A Double Nickase Plasmid (h): sc-418267-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- APOBEC3A 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
- APOBEC3A Double Nickase Plasmid (h) and APOBEC3A Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting APOBEC3A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APOBEC3A Double Nickase Plasmid (h) | sc-418267-NIC | 20 µg | $410.00 | |||
APOBEC3A Double Nickase Plasmid (h2) | sc-418267-NIC-2 | 20 µg | $410.00 |
Human APOBEC3A encodes a single-stranded DNA cytidine deaminase in the APOBEC family that catalyzes C-to-U editing and can generate mutations through replication and base-excision repair processing. APOBEC3A is induced by innate immune signaling, including interferon pathways, and contributes to cellular defense against viral genomes and endogenous retroelements. Its activity intersects with DNA damage response and genome maintenance processes, and dysregulated expression or mis-targeting is linked to characteristic mutational signatures observed in multiple cancer types. As a result, APOBEC3A is widely studied for its roles in antiviral restriction, inflammation-associated mutagenesis, and mechanisms of genomic instability.
APOBEC3A Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the APOBEC3A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within APOBEC3A. 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 APOBEC3A 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 APOBEC3A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.