RAD51AP1 Double Nickase Plasmid (h): sc-408187-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RAD51AP1 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
- RAD51AP1 Double Nickase Plasmid (h) and RAD51AP1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RAD51AP1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RAD51AP1 Double Nickase Plasmid (h) | sc-408187-NIC | 20 µg | $410.00 | |||
RAD51AP1 Double Nickase Plasmid (h2) | sc-408187-NIC-2 | 20 µg | $410.00 |
RAD51AP1 (RAD51 associated protein 1) is a DNA repair factor that interacts with RAD51 to promote homologous recombination during replication-associated damage and double-strand break repair. It supports RAD51-mediated strand invasion and D-loop formation, contributing to stabilization and restart of stalled replication forks and preservation of genome integrity. RAD51AP1 activity links to core DNA damage response processes, including S-phase checkpoint signaling and resolution of replication stress. Altered expression or function of RAD51AP1 has been associated with genomic instability phenotypes observed across multiple cancer types, making it a useful target for mechanistic studies of tumor cell DNA repair dependencies.
RAD51AP1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RAD51AP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RAD51AP1. 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 RAD51AP1 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 RAD51AP1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.