Rad51C Double Nickase Plasmid (h): sc-403060-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Rad51C 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
- Rad51C Double Nickase Plasmid (h) and Rad51C Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting RAD51C. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Rad51C Antibody (2H11): sc-56214
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rad51C Double Nickase Plasmid (h) | sc-403060-NIC | 20 µg | $410.00 | |||
Rad51C Double Nickase Plasmid (h2) | sc-403060-NIC-2 | 20 µg | $410.00 |
RAD51C encodes Rad51C, a RAD51 paralog that functions in homologous recombination and the Fanconi anemia–BRCA DNA repair network to resolve DNA double-strand breaks and interstrand crosslinks. Rad51C participates in RAD51 filament dynamics and Holliday junction processing, supporting replication fork stability and genome integrity during S/G2 phases. Disruption of RAD51C is associated with defective DNA damage responses, chromosomal instability, and increased sensitivity to genotoxic stress, making it a key node in pathways that govern replication stress tolerance. These properties link RAD51C to mechanisms underlying heritable cancer predisposition and DNA repair–related disorders, supporting its use in studying genome maintenance phenotypes.
Rad51C Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the RAD51C locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within RAD51C. 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 RAD51C 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 RAD51C-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.