Rad51D Double Nickase Plasmid (h): sc-408085-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Rad51D 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
- Rad51D Double Nickase Plasmid (h) and Rad51D Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RAD51D. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Rad51D Antibody (C-1): sc-398819
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rad51D Double Nickase Plasmid (h) | sc-408085-NIC | 20 µg | $410.00 | |||
Rad51D Double Nickase Plasmid (h2) | sc-408085-NIC-2 | 20 µg | $410.00 |
RAD51D encodes Rad51D, a RAD51 paralog that functions within the BCDX2 complex to promote homologous recombination (HR) and restart of stalled replication forks. Rad51D supports repair of DNA double-strand breaks, contributes to genome stability, and interfaces with the Fanconi anemia/BRCA network and checkpoint signaling during S and G2 phases. Defects in RAD51D impair HR capacity, elevate chromosomal instability, and are associated with hereditary cancer predisposition and tumorigenesis in multiple tissue contexts. As a result, RAD51D is widely studied in DNA damage response pathways, replication stress models, and structure–function analyses of HR mediator complexes.
Rad51D Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RAD51D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RAD51D. 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 RAD51D 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 RAD51D-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.