APOBEC3F Double Nickase Plasmid (h): sc-406610-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- APOBEC3F 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
- APOBEC3F Double Nickase Plasmid (h) and APOBEC3F Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting APOBEC3F. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APOBEC3F Double Nickase Plasmid (h) | sc-406610-NIC | 20 µg | $410.00 | |||
APOBEC3F Double Nickase Plasmid (h2) | sc-406610-NIC-2 | 20 µg | $410.00 |
Human APOBEC3F encodes a zinc-dependent cytidine deaminase that edits single-stranded DNA by converting cytidine to uridine, thereby introducing mutations that restrict replication of retroviruses and endogenous retroelements. As part of the APOBEC3 family, APOBEC3F participates in intrinsic immunity pathways that intersect with viral replication intermediates, DNA damage signaling, and genome surveillance. Its activity is modulated through interactions with viral antagonists such as HIV-1 Vif, linking APOBEC3F biology to host–pathogen arms races and viral escape mechanisms. Dysregulated or mistargeted deamination by APOBEC enzymes is also associated with mutational processes that can contribute to genome instability, making APOBEC3F a relevant factor for studies of mutation signatures and inflammatory microenvironments.
APOBEC3F Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the APOBEC3F locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within APOBEC3F. 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 APOBEC3F 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 APOBEC3F-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.